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Comprehensive Guide
Your thyroid is a small butterfly-shaped gland that controls your entire metabolism — energy, weight, body temperature, mood, cognition, and hormonal balance. This guide covers thyroid hormones (T3, T4, TSH, reverse T3), the supplements that support conversion and synthesis, the autoimmune thyroid connection, and how to optimize every aspect of thyroid function.
6
Thyroid markers to test
9
Evidence-based supplements
6
Clinical studies reviewed
20%
Of T4-to-T3 conversion occurs in the gut
Thyroid Basics
The thyroid is the master regulator of metabolism. Understanding the hormonal cascade is essential for knowing where things can go wrong — and where supplements can help.
Thyroid function involves a multi-step process from brain signaling to cellular metabolism. Each step is a potential point of dysfunction — and a potential intervention point.
Hypothalamus
Releases TRH (thyrotropin-releasing hormone) based on circulating thyroid hormone levels and metabolic demand
Pituitary
TRH stimulates the pituitary to release TSH (thyroid-stimulating hormone) into the bloodstream
Thyroid Gland
TSH signals the thyroid to uptake iodine and synthesize T4 (93%) and T3 (7%) using iodine + tyrosine
Peripheral Conversion
T4 is converted to active T3 (or inactive rT3) in the liver, kidneys, and gut by selenium-dependent deiodinase enzymes
Cellular Action
Free T3 enters cells, binds nuclear receptors, and activates genes controlling metabolism, energy, growth, and repair
The storage hormone — 93% of thyroid output
The active hormone — drives metabolism
Most thyroid dysfunction is not a production problem — it is a conversion problem. The thyroid may produce adequate T4, but without sufficient selenium, zinc, iron, and vitamin D, the body cannot efficiently convert T4 into the active T3 form. This is why many patients on levothyroxine (T4-only medication) still feel hypothyroid: they have plenty of T4 but poor conversion to T3. Optimizing the nutritional cofactors for T4-to-T3 conversion is often the single most impactful intervention for persistent thyroid symptoms.
Test Thoroughly
TSH alone is not enough. A comprehensive thyroid panel requires six markers to understand the full picture — including conversion efficiency, autoimmunity, and cellular function.
TSH
Thyroid Stimulating Hormone
Pituitary signal telling the thyroid to produce hormones. Rises when thyroid output is low (hypothyroid) and falls when output is high (hyperthyroid). The most commonly tested thyroid marker, but insufficient on its own.
Standard
0.45 – 4.5 mIU/L
Optimal
1.0 – 2.0 mIU/L
Many people feel best with TSH between 1.0-2.0. A TSH above 2.5 with symptoms warrants further investigation.
Free T4
Free Thyroxine
The primary hormone produced by the thyroid gland. T4 is a prohormone — it must be converted to T3 to become metabolically active. Represents thyroid gland output capacity.
Standard
0.82 – 1.77 ng/dL
Optimal
1.1 – 1.5 ng/dL
Free (unbound) T4 is more clinically useful than total T4. Low free T4 with elevated TSH confirms primary hypothyroidism.
Free T3
Free Triiodothyronine
The active thyroid hormone that drives metabolism, energy production, body temperature, and gene expression in virtually every cell. 80% is produced by peripheral conversion of T4 to T3 (primarily in liver and kidneys). The most metabolically important thyroid marker.
Standard
2.0 – 4.4 pg/mL
Optimal
3.0 – 4.0 pg/mL
Often not ordered by conventional doctors. If TSH and free T4 are 'normal' but free T3 is low, you may have a conversion problem.
Reverse T3
Reverse Triiodothyronine
Inactive form of T3 produced when the body needs to slow metabolism. Acts as a brake on thyroid function. Elevated in chronic stress, calorie restriction, inflammation, and illness.
Standard
9.2 – 24.1 ng/dL
Optimal
< 15 ng/dL
The free T3:reverse T3 ratio matters more than rT3 alone. Ratio should ideally be above 1.8 (same units).
TPO Antibodies
Thyroid Peroxidase Antibodies
Autoantibodies that attack the thyroid peroxidase enzyme, which is essential for thyroid hormone synthesis. Elevated TPO antibodies are the hallmark of Hashimoto’s thyroiditis — present in 90-95% of Hashimoto’s cases.
Standard
< 35 IU/mL
Optimal
< 10 IU/mL
Can be elevated years before TSH becomes abnormal. If TPO antibodies are present, autoimmune thyroid destruction has begun.
TG Antibodies
Thyroglobulin Antibodies
Autoantibodies targeting thyroglobulin, the protein scaffold used to synthesize thyroid hormones. Present in 60-80% of Hashimoto’s cases and in some cases of Graves’ disease.
Standard
< 40 IU/mL
Optimal
< 4 IU/mL
Some patients have elevated TG antibodies but normal TPO antibodies — testing both is important for complete autoimmune screening.
Important: Most conventional doctors only test TSH, and sometimes free T4. This misses conversion problems (low free T3), autoimmune activity (TPO and TG antibodies), and metabolic braking (elevated reverse T3). Request the full 6-marker panel for a complete picture. Many direct-to-consumer lab services offer comprehensive thyroid panels without a doctor’s order.
Targeted Support
These supplements address the nutritional cofactors required for thyroid hormone synthesis, T4-to-T3 conversion, autoimmune modulation, and cellular thyroid receptor function. Ranked by evidence tier.
150 – 300 mcg/day (from kelp or potassium iodide)
Iodine is the essential building block of thyroid hormones — T4 contains four iodine atoms and T3 contains three. Without adequate iodine, the thyroid cannot synthesize hormones, leading to compensatory TSH elevation and eventually goiter (thyroid enlargement). The thyroid actively concentrates iodine to 20-40x serum levels via the sodium-iodide symporter (NIS). Iodine deficiency remains the leading cause of preventable hypothyroidism worldwide, affecting approximately 2 billion people.
Always pair iodine with selenium to protect against oxidative damage from iodine metabolism. Excess iodine (> 1,100 mcg/day) can paradoxically suppress thyroid function (Wolff-Chaikoff effect) or worsen Hashimoto’s. Test urinary iodine before high-dose supplementation. Seaweed sources vary wildly in iodine content — kelp can range from 100 to 2,000+ mcg per gram.
200 mcg/day
Cofactor for three critical thyroid enzyme families: deiodinases (D1, D2, D3) that convert T4 to T3; glutathione peroxidases that neutralize H2O2 produced during thyroid hormone synthesis; and thioredoxin reductases that regulate thyroid cell redox status. Multiple RCTs demonstrate 200 mcg/day selenomethionine reduces TPO antibodies by 40-50% in Hashimoto’s patients over 6-12 months. The thyroid contains more selenium per gram than any other organ.
Selenomethionine is the best-absorbed form. Do not exceed 400 mcg/day — selenium toxicity (selenosis) causes hair loss, nail brittleness, and GI symptoms. Brazil nuts are the richest food source (68-91 mcg per nut), but content varies by soil. Blood selenium level of 120-150 ng/mL is optimal.
25 – 30 mg/day (as zinc picolinate or bisglycinate)
Zinc is required for the synthesis of thyroid-releasing hormone (TRH) in the hypothalamus and for T3 binding to its nuclear receptor. Zinc deficiency impairs both thyroid hormone production and the peripheral action of thyroid hormones. A study in the American Journal of Clinical Nutrition showed that zinc supplementation in zinc-deficient hypothyroid patients improved T3 levels by 12.6%. Zinc also supports the conversion of T4 to T3 and is essential for over 300 enzymatic reactions including immune function.
Always balance zinc with copper (2 mg copper per 30 mg zinc) to prevent copper depletion. Take with food to avoid nausea. Zinc competes with iron for absorption — separate doses by 2 hours. Zinc carnosine is preferred if you also have gut issues. Test RBC zinc for the most accurate assessment.
5,000 IU D3 + 100-200 mcg K2 (MK-7) daily
Vitamin D deficiency is strongly associated with autoimmune thyroid disease. Studies show that patients with Hashimoto’s have significantly lower vitamin D levels than controls, and that vitamin D supplementation reduces TPO antibodies. Vitamin D modulates the immune system by promoting T-regulatory cells (which prevent autoimmunity) and suppressing Th17 cells (which drive autoimmune destruction). A meta-analysis found that each 5 ng/mL increase in 25(OH)D was associated with a significant reduction in thyroid antibody levels.
Target blood level: 50-80 ng/mL (125-200 nmol/L). Most hypothyroid patients are deficient (< 30 ng/mL). K2 ensures calcium is deposited in bones, not arteries. Take with fat-containing meal for absorption. Test 25(OH)D every 3 months until stable.
18 – 36 mg/day if deficient (based on ferritin levels)
Iron is a cofactor for thyroid peroxidase (TPO), the enzyme that catalyzes the iodination of tyrosine residues to form thyroid hormones. Iron deficiency impairs TPO activity, reduces T4 production, and blunts the TSH response. Low ferritin (< 40 ng/mL) is associated with suboptimal thyroid function even when TSH appears normal. Studies show that correcting iron deficiency in hypothyroid patients improves the efficacy of thyroid hormone medication. Iron deficiency also impairs T4-to-T3 conversion in peripheral tissues.
Check ferritin before supplementing — optimal is 70-100 ng/mL for thyroid function. Iron bisglycinate is the best-tolerated form with fewer GI side effects. Take with vitamin C (200 mg) to enhance absorption by up to 6x. Separate from thyroid medication, calcium, and zinc by at least 4 hours. Do not supplement iron if ferritin is already adequate — excess iron is inflammatory and pro-oxidant.
300 – 600 mg/day standardized root extract
Adaptogenic herb that modulates the hypothalamic-pituitary-thyroid (HPT) axis. The landmark Sharma et al. (2018) RCT demonstrated that 600 mg/day of ashwagandha root extract for 8 weeks significantly increased serum T4 by 19.6% and normalized TSH in subclinical hypothyroid patients. Ashwagandha reduces cortisol by 28-30%, which is significant because chronic cortisol elevation suppresses TSH secretion, inhibits T4-to-T3 conversion, and increases reverse T3 production. By lowering cortisol, ashwagandha indirectly supports the entire thyroid hormone cascade.
KSM-66 and Sensoril are the best-studied standardized extracts. Contraindicated in hyperthyroidism (Graves’ disease) as it may further stimulate thyroid function. May be contraindicated in autoimmune conditions in some individuals — as an immune stimulant, it could theoretically worsen Hashimoto’s in some people. Nightshade family — avoid if you have nightshade sensitivity. Start with 300 mg and increase gradually.
B12: 1,000 mcg methylcobalamin; B6: 50 mg P-5-P; Folate: 400 mcg methylfolate
B12 deficiency is found in up to 40% of hypothyroid patients, particularly those with Hashimoto’s (autoimmune thyroid often co-occurs with pernicious anemia and autoimmune gastritis). B6 is a cofactor for the conversion of T4 to T3. Methylfolate supports methylation pathways that regulate thyroid hormone metabolism and homocysteine clearance. Elevated homocysteine (common in hypothyroidism) is an independent cardiovascular risk factor and indicates impaired methylation that affects hormone processing.
Use methylated forms (methylcobalamin, methylfolate, P-5-P) for optimal bioavailability, especially if you have MTHFR polymorphisms. Hypothyroid patients on levothyroxine often have impaired B12 absorption due to low stomach acid (achlorhydria). Sublingual B12 bypasses the need for intrinsic factor. Test serum B12, homocysteine, and methylmalonic acid for complete B12 status assessment.
500 – 1,000 mg/day on an empty stomach
Tyrosine is the amino acid backbone of thyroid hormones. T4 (thyroxine) is literally two tyrosine molecules bonded together with four iodine atoms. While outright tyrosine deficiency is rare, stress-induced depletion can impair thyroid hormone synthesis and neurotransmitter production (tyrosine is also a precursor to dopamine and norepinephrine). Supplementation may benefit individuals under chronic stress who are diverting tyrosine toward catecholamine production at the expense of thyroid hormone synthesis.
Most relevant for individuals under chronic stress or on restrictive diets low in protein. Take on an empty stomach for best absorption (competes with other large neutral amino acids for transport across the blood-brain barrier). Contraindicated in hyperthyroidism and in patients taking MAO inhibitors. Limited RCT evidence specifically for thyroid function — mechanism is plausible but clinical trials are sparse.
300 – 400 mg elemental magnesium daily
Magnesium is required for the conversion of T4 to the active T3 form. Deficiency (affecting 50%+ of the population) impairs this conversion and is associated with higher rates of Hashimoto’s thyroiditis. Magnesium also regulates the HPA axis — deficiency increases cortisol, which suppresses thyroid function. Additionally, magnesium is critical for vitamin D metabolism; without adequate magnesium, vitamin D remains in its inactive form, compounding the D-thyroid connection.
Glycinate for calming and sleep support. Malate for energy and mitochondrial function. Avoid magnesium oxide (poor absorption, GI distress). Split dose between morning and evening. Separate from thyroid medication by 4 hours. RBC magnesium is a more accurate test than serum magnesium — optimal is 5.5-6.5 mg/dL.
Disclaimer: Supplements are not a replacement for thyroid medication or medical treatment. Always consult your healthcare provider before starting a new supplement regimen, especially if you take thyroid medication or have an existing thyroid condition. The information here is educational, not prescriptive. See our full disclaimer.
Want This Personalized?
This guide gives you the science. A CryoCove coach gives you the personalization — the right dose, timing, and integration with your other 8 pillars.
Autoimmune Thyroid
Hashimoto's thyroiditis is the most common cause of hypothyroidism in the developed world. It is an autoimmune condition where the immune system attacks and gradually destroys the thyroid gland.
The goal in Hashimoto’s is not just thyroid hormone replacement — it is to reduce the autoimmune attack on the thyroid, preserve remaining thyroid tissue, and address the root causes driving immune dysregulation.
Dietary Considerations
Goitrogens are naturally occurring compounds in certain foods that can interfere with thyroid function. Understanding the nuance matters — most people do not need to eliminate these foods entirely.
Foods: Broccoli, cauliflower, kale, Brussels sprouts, cabbage, bok choy, collard greens, turnips
Compound
Glucosinolates → isothiocyanates and thiocyanates
Mechanism
Thiocyanates compete with iodine for uptake via the sodium-iodide symporter (NIS), reducing raw material for thyroid hormone synthesis. Goitrin directly inhibits thyroid peroxidase.
Mitigation
Cooking reduces goitrogenic activity by 30-80%. Steaming for 3-5 minutes is sufficient. Do not consume large quantities raw (juicing raw kale daily is the main concern). Ensure adequate iodine intake.
Foods: Tofu, tempeh, soy milk, edamame, soy protein isolate, soy-based infant formula
Compound
Isoflavones (genistein, daidzein)
Mechanism
Soy isoflavones inhibit thyroid peroxidase (TPO) and may block the absorption of synthetic thyroid hormone medication. Genistein specifically has been shown to reduce T4 production in vitro.
Mitigation
Moderate fermented soy (tempeh, miso) is generally safe. Avoid soy protein isolate and unfermented soy in large quantities if hypothyroid. Separate soy intake from thyroid medication by at least 4 hours. Impact is most significant in iodine-deficient individuals.
Foods: Pearl millet, finger millet, proso millet
Compound
C-glycosylflavones
Mechanism
Flavonoids in millet inhibit thyroid peroxidase even more potently than soy isoflavones in some studies. Particularly relevant in regions where millet is a dietary staple.
Mitigation
Avoid millet as a staple grain if hypothyroid. Occasional consumption is unlikely to be problematic. Less relevant in Western diets where millet consumption is typically low.
Foods: Strawberries, peaches, pears, cassava, sweet potatoes, lima beans
Compound
Various cyanogenic glycosides (cassava), flavonoids (fruits)
Mechanism
Cyanogenic glycosides in cassava release thiocyanate when metabolized. Fruit-based goitrogens are much weaker and clinically insignificant at normal dietary intake.
Mitigation
Cook cassava thoroughly (boiling removes most cyanogenic compounds). Fruit consumption is safe for virtually all thyroid patients — the goitrogenic content is negligible relative to the nutritional benefits.
Bottom line: The anti-cancer and detoxification benefits of cruciferous vegetables far outweigh the thyroid risk for most people. Cook your cruciferous vegetables, ensure adequate iodine intake, and avoid consuming large quantities of raw goitrogenic foods (e.g., daily raw kale smoothies with 3-4 cups of kale). Soy is the most relevant goitrogen to manage if you have hypothyroidism — especially unfermented soy products and soy protein isolate.
The Gut Connection
Your gut and thyroid are intimately connected. Gut health directly affects thyroid hormone conversion, autoimmunity risk, and medication absorption.
Approximately 20% of T4-to-T3 conversion occurs in the gastrointestinal tract, mediated by intestinal sulfatase enzymes and the action of beneficial gut bacteria. Dysbiosis (microbial imbalance) reduces this conversion, lowering active T3 levels. Certain Lactobacillus and Bifidobacterium species specifically support thyroid hormone metabolism.
70% of the immune system resides in gut-associated lymphoid tissue (GALT). Intestinal permeability allows undigested food proteins, bacterial endotoxins (LPS), and other antigens to enter the bloodstream, triggering systemic immune activation. The gliadin protein in gluten has molecular similarity to thyroid tissue — the immune system may attack both (molecular mimicry).
Levothyroxine absorption occurs primarily in the jejunum and ileum. GI conditions including celiac disease, H. pylori infection, atrophic gastritis, lactose intolerance, and small intestinal bacterial overgrowth (SIBO) all impair levothyroxine absorption, leading to inadequate thyroid hormone levels despite appropriate dosing.
A healthy gut is required for absorption of all thyroid-supporting nutrients: iodine, selenium, zinc, iron, vitamin D, and B12. Gut inflammation, low stomach acid (common in hypothyroidism), and dysbiosis reduce nutrient bioavailability, creating a vicious cycle where poor gut health leads to poor thyroid support and vice versa.
The Stress Connection
Chronic stress is one of the most overlooked causes of thyroid dysfunction. The adrenal glands and thyroid are deeply interconnected — you cannot optimize one without addressing the other.
Cortisol (your primary stress hormone) affects thyroid function at every level of the HPT axis. In acute stress, this is protective. In chronic stress, it becomes destructive.
TSH transiently suppressed, T4-to-T3 conversion reduced, reverse T3 increases. This is a protective mechanism to conserve energy during acute threat.
Sustained TSH suppression, chronic T3 depletion, elevated rT3, increased thyroid antibodies (stress-induced immune dysregulation). Functional hypothyroidism develops despite 'normal' TSH. Leptin and insulin resistance compound metabolic slowdown.
Without adequate cortisol, cells cannot respond to thyroid hormones properly. Starting thyroid medication without addressing adrenal dysfunction can worsen fatigue and anxiety. The adrenals must be supported before or alongside thyroid treatment.
Critical insight: If you start thyroid medication or thyroid-supporting supplements without first addressing adrenal dysfunction, you may feel worse. Increasing thyroid hormones raises metabolic demand, but if the adrenals cannot meet that demand (due to cortisol depletion), the result is increased anxiety, heart palpitations, and fatigue. Always address adrenal health alongside thyroid optimization.
Practical Application
Timing supplements around thyroid medication is critical. Many common supplements interfere with thyroid medication absorption. This schedule optimizes both medication efficacy and supplement absorption.
Thyroid medication only (levothyroxine, Synthroid, Armour, NP Thyroid)
Empty stomach, full glass of water. Nothing else for 60 minutes.
Vitamin D3 + K2, Ashwagandha, B-Complex
Fat-soluble vitamins need dietary fat for absorption. Ashwagandha and B vitamins do not interfere with thyroid medication at this interval.
Zinc, Magnesium (half dose), L-Tyrosine (if using)
Zinc with food to prevent nausea. Keep zinc separate from iron by 2+ hours. L-Tyrosine can be taken on an empty stomach 30 min before lunch for best absorption.
Iron (if needed) + Vitamin C, Selenium, Iodine
Iron absorbs best with vitamin C and away from calcium, zinc, and thyroid medication. Selenium and iodine work synergistically and are well-absorbed with an evening meal.
Magnesium (second half dose)
Magnesium glycinate promotes relaxation and sleep. Separate from thyroid medication by 4+ hours if you take your medication in the morning.
The following must be separated from levothyroxine (Synthroid, Tirosint) by at least 4 hours:
Alternative approach: Some endocrinologists recommend taking thyroid medication at bedtime (at least 3 hours after the last meal and supplements). Studies show that bedtime dosing actually improves absorption compared to morning dosing because the stomach is truly empty. This eliminates the morning timing complexity and allows you to take all supplements freely during the day. Discuss this option with your prescribing physician.
The Evidence
The recommendations in this guide are based on peer-reviewed clinical studies. Here are the key studies informing our supplement recommendations.
Toulis et al. (2010) — Meta-analysis
Thyroid, 20(10), 1163-1173
Key Finding
Meta-analysis of randomized controlled trials found that 200 mcg/day selenomethionine significantly reduced TPO antibody levels in Hashimoto’s patients at 3, 6, and 12 months compared to placebo, with a weighted mean difference of approximately -271 IU/mL at 12 months.
Clinical significance: Established selenium as the most evidence-based supplement for autoimmune thyroid disease. Effect size is clinically meaningful and consistent across multiple trials.
Sharma, Basu, & Singh (2018)
Journal of Alternative and Complementary Medicine, 24(3), 243-248
Key Finding
Double-blind RCT of 50 participants with subclinical hypothyroidism. 600 mg ashwagandha root extract daily for 8 weeks significantly improved TSH (p<0.001), serum T3 (p<0.01), and T4 levels (p<0.001) compared to placebo. T4 increased by approximately 19.6%.
Clinical significance: First rigorous RCT demonstrating an herbal adaptogen can meaningfully improve thyroid function in subclinical hypothyroidism. TSH normalized in the ashwagandha group.
Wang et al. (2015) — Meta-analysis
International Journal of Clinical and Experimental Medicine, 8(9), 15419-15425
Key Finding
Meta-analysis of 20 studies found that patients with autoimmune thyroid disease had significantly lower 25(OH)D levels than healthy controls (OR 2.99 for vitamin D deficiency). Vitamin D supplementation in interventional studies reduced TPO antibody titers.
Clinical significance: Establishes a strong association between vitamin D deficiency and autoimmune thyroid disease, supporting vitamin D optimization as part of Hashimoto’s management.
Zimmermann & Köhrle (2002)
Thyroid, 12(10), 867-878
Key Finding
Iron deficiency reduced thyroid peroxidase activity by 50-80% in animal models and impaired T4 production. In human studies, iron-deficient women had impaired thyroid hormone synthesis even with adequate iodine, and iron supplementation improved thyroid function indices (p<0.05).
Clinical significance: Demonstrates that iron status must be assessed alongside thyroid function. Iron deficiency is a commonly overlooked cause of persistent hypothyroid symptoms despite medication.
Knezevic et al. (2020) — Systematic Review
Frontiers in Endocrinology, 11, 586893
Key Finding
Systematic review demonstrated that gut dysbiosis is significantly associated with autoimmune thyroid disease. Intestinal bacteria contribute to approximately 20% of peripheral T4-to-T3 conversion. Probiotic supplementation (Lactobacillus and Bifidobacterium strains) showed preliminary improvement in thyroid function markers.
Clinical significance: Establishes the gut-thyroid axis as a clinically relevant pathway. Supports gut health optimization as part of comprehensive thyroid management.
Nishiyama et al. (1994)
Journal of the American College of Nutrition, 13(1), 62-67
Key Finding
Zinc supplementation (26.4 mg/day) in mildly zinc-deficient patients significantly increased free T3 and free T4 levels while normalizing elevated rT3. The T3:rT3 ratio improved significantly (p<0.05), suggesting improved peripheral conversion efficiency.
Clinical significance: Early but important evidence that zinc deficiency impairs T4-to-T3 conversion and increases reverse T3 production. Supports zinc testing and supplementation in thyroid patients.
Your Action Plan
A step-by-step approach to supporting thyroid health. Build the foundation first, then layer in targeted interventions based on your lab results.
Weeks 1-4 — Test and establish baseline
The goal is to establish your baseline, identify deficiencies, and start the most foundational supplements. Selenium alone can begin improving T4-to-T3 conversion and reducing antibodies within 4-8 weeks.
Weeks 5-12 — Address deficiencies and support conversion
This phase addresses specific deficiencies identified in your baseline labs and begins healing the gut-thyroid axis. Most people experience meaningful improvement in energy, body temperature, and cognitive clarity by week 8-12.
Month 4+ — Full optimization and maintenance
At this level, you are optimizing the full thyroid ecosystem: production, conversion, cellular sensitivity, autoimmune modulation, gut health, and adrenal support. Track your biomarkers quarterly and adjust based on results — thyroid optimization is an ongoing process, not a one-time fix.
FAQ
Biomarkers
Track thyroid markers alongside metabolic, inflammatory, and hormonal biomarkers for complete health optimization.
Inflammation
Chronic inflammation drives autoimmune thyroid disease. Learn how to measure and reduce inflammatory markers.
Gut Health
20% of T4-to-T3 conversion happens in the gut. Heal your gut to optimize thyroid function.
This guide gives you the science. A CryoCove coach gives you the personalization — which labs to run, which supplements to prioritize based on your results, how to time everything around your medication, and ongoing accountability as your thyroid markers improve.