Thyroid

This marker sits in Sense -- signals being produced, detected and acted on.

A pituitary hormone that rises or falls to tell the thyroid gland to make more or less T4/T3; because the pituitary responds to even small changes in circulating thyroid hormone, TSH is the most sensitive single screening marker for thyroid over- or under-activity.

Typical range: Conventional lab range: roughly 0.4-4.5 mIU/L (varies by lab/assay). The National Academy of Clinical Biochemistry has argued the reference interval should be narrower, closer to 0.4-2.5 mIU/L, based on the TSH distribution in a disease-free NHANES III subgroup, but the American Thyroid Association and Endocrine Society have not adopted this as the official diagnostic cutoff, and mainstream guidance still treats 4.5-10 mIU/L as "subclinical" rather than automatically treatable. Functional optimal (opinion): 1.0-2.0 mIU/L is commonly cited by functional-medicine practitioners as ideal -- this is an opinion range, not an official diagnostic target. (cite: review of TSH reference-range debate, PMC6778876)

Food first: Adequate iodine (iodized salt, dairy, seafood) without megadosing; selenium sufficiency (1-2 Brazil nuts/day or 55-200 mcg/day) in deficient or autoimmune contexts.

When to see someone: A single TSH can be skewed by acute illness, a recent iodine load such as imaging contrast dye, time of day, and **biotin supplements, which interfere with many TSH immunoassays** -- if you take biotin, say so before the draw, since it can make the result look convincingly wrong.

This marker sits in Sense -- signals being produced, detected and acted on.

The unbound, biologically available fraction of T4, the storage/precursor form of thyroid hormone that tissues convert to the more active T3 as needed.

Typical range: Conventional: roughly 0.8-1.8 ng/dL (assay-dependent). Functional optimal (opinion): upper-middle of the range is often preferred by functional practitioners, particularly in symptomatic patients with a low-normal TSH -- this is opinion, not an official target, and Free T4 is meant to be interpreted alongside TSH, not in isolation.

Food first: Ensure adequate iodine, selenium, iron, and zinc through diet (seafood, eggs, dairy, meat, nuts, seeds). Correcting an underlying deficiency, if present, is the evidence-based lever -- supplementing beyond sufficiency has not been shown to raise Free T4 further in replete people.

When to see someone: If you are on levothyroxine, dose is titrated to TSH and Free T4 together, and changing mineral intake around your medication timing can shift the reading independent of true thyroid status -- worth telling whoever manages your dose.

This marker sits in Sense -- signals being produced, detected and acted on.

The combined bound-plus-unbound (free) T4 in blood; because ~99% of T4 travels bound to thyroid-binding globulin (TBG) and other carrier proteins, Total T4 is heavily influenced by anything that changes carrier-protein levels (pregnancy, oral estrogen/birth control, liver disease), which is why Free T4 is now favored clinically.

Typical range: Conventional: roughly 5.0-12.0 mcg/dL (lab-dependent). No widely used functional-medicine "optimal" range is applied separately from Free T4, since Total T4 is the less specific of the two.

Food first: Same levers as Free T4 -- adequate iodine is the dominant nutritional driver of total hormone output.

When to see someone: Total T4 moves with binding-protein changes (pregnancy, estrogen therapy, liver or kidney disease) even when actual thyroid function is normal -- don't interpret it without Free T4 and TSH alongside it.

This marker sits in Sense -- signals being produced, detected and acted on.

The unbound, biologically active thyroid hormone that actually acts on tissue receptors; most circulating T3 is made by peripheral conversion of T4 rather than direct thyroid secretion, so Free T3 partly reflects conversion efficiency, not just gland output.

Typical range: Conventional: roughly 2.3-4.2 pg/mL (lab-dependent). Functional optimal (opinion): upper-middle of range is often preferred; not an official target.

Food first: Correct any underlying selenium, iron, or zinc deficiency through diet or targeted, tested supplementation; extreme calorie restriction and acute illness both lower Free T3 independent of nutrient status (a physiological down-regulation, not a deficiency to chase with supplements).

When to see someone: Low Free T3 in the setting of illness ("euthyroid sick syndrome" / non-thyroidal illness syndrome) is a normal adaptive response, not something to correct with iodine or thyroid supplements -- treating it as a deficiency in an acutely ill person can do harm.

This marker sits in Sense -- signals being produced, detected and acted on.

Combined bound-plus-free T3; like Total T4, it moves with carrier-protein status as well as true thyroid hormone output.

Typical range: Conventional: roughly 80-200 ng/dL (lab-dependent). No separate functional "optimal" range beyond what's used for Free T3.

Food first: Same as Free T3.

When to see someone: Total T3 is rarely used alone clinically (Free T3 and TSH are preferred); interpret cautiously in pregnancy or with estrogen therapy, which raise binding globulin and inflate Total T3/T4 without reflecting true thyroid status.

This marker sits in Sense -- signals being produced, detected and acted on.

An inactive mirror-image form of T3 that the body makes from T4 instead of active T3, especially under stress, illness, fasting, or high cortisol -- it's thought of as a "brake" the body applies to slow metabolism when resources are scarce.

Typical range: Conventional: roughly 9.2-24.1 ng/dL (Labcorp) or 10-24 ng/dL (Quest), assay-dependent. Functional/integrative practitioners sometimes cite an "optimal" range of 9.2-14.0 ng/dL (the lower portion of the standard interval), but this is a practitioner-community opinion, not a validated clinical target -- mainstream endocrinology does not use rT3 for routine thyroid management and reserves it mainly for research contexts like distinguishing non-thyroidal illness syndrome from true hypothyroidism.

Food first: Address underlying iron or selenium deficiency if present; manage the actual physiological stressor (acute illness, severe calorie restriction, overtraining, chronic sleep deprivation) that's driving the T4-to-rT3 shift, since rT3 is usually a downstream signal of stress physiology rather than a standalone nutrient deficiency to chase.

When to see someone: Reverse T3 is not part of standard endocrinology practice for diagnosing or monitoring hypothyroidism, and treating an elevated rT3 with thyroid hormone in someone with normal TSH/Free T4 is not evidence-based and can cause iatrogenic hyperthyroidism. Don't let a single rT3 number drive a treatment decision without an endocrinologist involved.

This marker sits in Sense -- signals being produced, detected and acted on.

A calculated ratio (Free T3 divided by rT3, sometimes rescaled x10 or x100 depending on units) that functional and integrative practitioners use as a proxy for how much of the body's T4 is being converted to active hormone versus the inactive "brake" form.

Typical range: No official clinical reference range exists. Functional-medicine sources commonly describe a ratio above roughly 0.2 (in pg/mL over ng/dL units) as "optimal," with some versions of the calculation (different unit scaling) citing a target above 20. **This ratio is not validated in peer-reviewed clinical trials and is not endorsed by the American Thyroid Association, Endocrine Society, or mainstream lab medicine** -- treat any specific cutoff as a community convention, not a clinical standard.

Food first: There is no nutrition protocol proven in controlled trials to specifically move this ratio; the practical approach is to address the individual T3, rT3, iron, and selenium levels the ratio is built from, using the evidence available for each of those markers separately.

When to see someone: Be cautious with any practitioner who bases a treatment plan primarily on this ratio -- it's a popular functional-medicine heuristic, not a peer-reviewed diagnostic tool, and shouldn't override TSH/Free T4/Free T3 in isolation, let alone a clinical exam.

This marker sits in Sense -- signals being produced, detected and acted on.

Antibodies against thyroid peroxidase, the enzyme that iodinates thyroglobulin to build thyroid hormone; elevated TPOAb is the single best marker of underlying autoimmune thyroid disease (Hashimoto's thyroiditis, and it's also positive in a meaningful share of Graves' patients).

Typical range: Conventional: typically <35 IU/mL (varies significantly by lab/assay, from <9 to <60 IU/mL depending on platform). Roughly 10-15% of people with no clinical thyroid disorder have a mildly positive TPOAb. There is no separate "functional optimal" range beyond negative/very low -- some functional-medicine sources describe an aspirational target of <9 IU/mL, but this is a low-quality-sourced opinion, not a validated clinical target, and should not be treated as an evidence-based goal distinct from the standard negative cutoff.

Food first: Selenium sufficiency (dietary or a time-limited 200 mcg/day supplement) is the most evidence-backed nutrient lever specifically for TPOAb in diagnosed autoimmune thyroiditis; correcting a confirmed vitamin D, iron, or magnesium deficiency is reasonable supportive care if one of those is actually low on testing.

When to see someone: Selenium's antibody-lowering effect is strongest at 3-6 months and can fade with longer use in some trials -- it should be time-limited and monitored, not taken indefinitely at high doses. None of these nutrients reverse or cure autoimmune thyroiditis; they are adjuncts to standard management, not replacements for it.

Antibodies against thyroglobulin, the protein thyroid cells use as a scaffold to build hormone; elevated TgAb is seen in both Hashimoto's and Graves' disease, and is checked routinely alongside thyroglobulin testing in thyroid cancer follow-up because TgAb positivity can make thyroglobulin readings unreliable (see Thyroglobulin entry below).

Typical range: Conventional: typically <1 to ~4 IU/mL depending on assay/lab (negative cutoff is assay-specific). No separate "functional optimal" range beyond negative/normal.

Food first: Selenium sufficiency is the most evidence-backed lever specifically for antibody levels; addressing a confirmed vitamin D or magnesium deficiency is reasonable supportive care.

When to see someone: A positive TgAb can make thyroglobulin (Tg) testing unreliable as a cancer-recurrence marker (falsely low Tg readings) -- always order TgAb alongside Tg in thyroid cancer follow-up, and flag a positive TgAb to the ordering clinician rather than interpreting Tg alone.

This marker sits in Sense -- signals being produced, detected and acted on.

Antibodies that bind the TSH receptor on thyroid cells; in Graves' disease these antibodies mimic TSH and drive the gland to overproduce hormone. TSI specifically measures the stimulating subtype; TRAb (sometimes reported as TBII) measures total receptor-binding antibody activity, which can be stimulating, blocking, or neutral.

Typical range: Conventional: TSI reference range roughly 0.00-0.55 IU/L, with diagnostic cutoffs for Graves' commonly set around 0.55-1.3 IU/L depending on assay and desired sensitivity/specificity balance; TRAb reference range roughly 0.00-1.75 IU/L, with some automated assays using cutoffs closer to 1.56-2.89 IU/L. These are qualitative/diagnostic tests for autoimmune hyperthyroidism, not continuous wellness markers with a "functional optimal" range.

Food first: Selenium sufficiency is reasonable supportive care specifically in mild Graves' orbitopathy alongside standard endocrinology/ophthalmology management, not as a substitute for it.

When to see someone: Graves' disease requires medical management (antithyroid drugs, radioactive iodine, or surgery) -- supplements are, at best, adjunctive for the eye-disease component and should never be used to try to manage hyperthyroidism itself, which carries real cardiac risk if untreated.

The protein scaffold thyroid cells use to synthesize and store thyroid hormone; in someone with an intact thyroid it's a rough marker of thyroid tissue mass and iodine status, but its main clinical use is as a tumor marker after thyroidectomy for differentiated thyroid cancer, where it's tracked to detect recurrence.

Typical range: Conventional: roughly 3-40 ng/mL in euthyroid people with an intact thyroid and a negative TgAb, in iodine-sufficient populations (assay standardized to the CRM-457 reference material). This range does not apply post-thyroidectomy: after total thyroidectomy for cancer, Tg 0.1-2.0 ng/mL on suppressive therapy suggests low recurrence risk, while Tg ≥10 ng/mL on suppression suggests a >25% risk of clinically detectable recurrence; TSH-stimulated Tg below 1.0 ng/mL (American Thyroid Association) or 0.5 ng/mL (British Thyroid Association) is associated with a 98-99.5% probability of being cancer-free.

Food first: In someone with an intact thyroid and no cancer history, adequate iodine and vitamin A status support normal thyroglobulin/TSH regulation; this is not a marker to try to move deliberately outside of that basic sufficiency picture.

When to see someone: A rising thyroglobulin after thyroidectomy for cancer needs prompt oncologic/endocrine follow-up, not a nutrition intervention. Thyroglobulin results are unreliable in the presence of TgAb (false-low readings) -- always check TgAb status before trusting a Tg number.

This marker sits in Exchange -- moving iron across boundaries and handing it between carriers.

Typical range: Conventional ferritin: roughly 15-150 ng/mL (women), 20-250 ng/mL (men), lab-dependent. Functional-medicine practitioners frequently cite ferritin in the 90-100+ ng/mL range as a better target for optimal thyroid hormone conversion than the low end of the standard range -- this specific numeric target is a commonly circulated functional-medicine opinion, not a number validated in a dedicated RCT, even though iron's underlying mechanistic role in TPO/deiodinase function is well established.

Food first: Heme iron (red meat, poultry, fish) is more bioavailable than plant (non-heme) iron; pair plant iron sources with vitamin C to improve absorption. Correcting a confirmed iron deficiency is the evidence-based lever -- supplementing iron in someone who is already iron-replete has no established thyroid benefit.

When to see someone: Iron is the mineral where confirming the deficiency first genuinely matters. Overload causes real and irreversible damage to the liver, heart and pancreas, and hereditary haemochromatosis affects roughly 1 in 200 people of Northern European ancestry. Ferritin also rises with inflammation, so it can read falsely normal in someone who is both deficient and inflamed -- read it alongside iron saturation, TIBC and CRP rather than alone. If you take levothyroxine, iron blocks its absorption when taken too close together; separate them.

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

Typical range: Conventional serum range roughly 60-120 mcg/dL (assay-dependent); RDA 11 mg/day (men), 8 mg/day (women).

Food first: Oysters (richest source), red meat, poultry, beans, nuts, seeds, dairy; correcting a confirmed zinc deficiency (via serum zinc testing) is the evidence-based approach rather than empiric high-dose supplementation.

When to see someone: Chronic zinc supplementation above 40 mg/day can cause copper deficiency (zinc and copper compete for absorption), leading to anemia and neurological problems -- balance any sustained zinc use with adequate copper intake or monitoring.

This marker sits in Build -- the raw material for making and renewing structure.

Typical range: Conventional (Endocrine Society): deficient <20 ng/mL, insufficient 20-29 ng/mL, sufficient ≥30 ng/mL. Functional optimal (opinion): 40-60 ng/mL is widely cited by functional-medicine practitioners, but the Endocrine Society's 2024 update explicitly declined to set an outcome-specific optimal target for healthy adults -- treat "40-60" as opinion, not consensus. (cite: Endocrine Society Clinical Practice Guideline update, 2024)

Food first: Fatty fish, egg yolks, fortified dairy, sensible sun exposure; supplementation (typically 1,000-4,000 IU/day) is often needed to reach sufficiency, and correcting a confirmed deficiency is the most defensible target in someone with diagnosed autoimmune thyroid disease.

When to see someone: Vitamin D toxicity is rare but real at sustained doses above 10,000 IU/day without monitoring, causing hypercalcemia. People with granulomatous disease or hyperparathyroidism need medical supervision before supplementing.

This marker sits in Build -- the raw material for making and renewing structure.

Typical range: No functional-medicine "optimal" range is commonly cited for vitamin A in the thyroid context specifically; standard serum retinol reference ranges are roughly 20-60 mcg/dL (adult), RDA 900 mcg RAE/day (men), 700 mcg RAE/day (women).

Food first: This evidence base is strongest in populations with combined iodine and vitamin A deficiency (common in parts of the developing world) -- it does not establish that vitamin A supplementation benefits thyroid function in vitamin-A-replete adults in iodine-sufficient regions. Food sources: liver, eggs, dairy, and orange/dark-green produce (as provitamin A carotenoids).

When to see someone: Preformed vitamin A (retinol, as opposed to beta-carotene) is fat-soluble and accumulates -- chronic high-dose supplementation can cause liver toxicity and, in pregnancy, birth defects at high doses. This is not a nutrient to megadose empirically; correct a confirmed deficiency rather than supplementing preventively at high doses.

Typical range: Tyrosine is not a routine clinical thyroid-panel test; it's occasionally measured in specialized amino acid/metabolic panels (reference ranges vary by lab), but there's no standard "thyroid workup" tyrosine level to target.

Food first: Adequate total dietary protein (meat, fish, eggs, dairy, soy, legumes) reliably supplies tyrosine; there is no evidence-based reason to add a standalone tyrosine supplement on top of adequate protein intake for thyroid support specifically.

When to see someone: L-tyrosine supplements are sometimes marketed for thyroid and adrenal/energy support -- treat these claims skeptically given the thin supplementation evidence. Tyrosine supplements can interact with MAOI antidepressants and thyroid medication absorption timing deserves the same caution as other supplements (see Medication Interactions below).

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

Typical range: Conventional: 1.7-2.2 mg/dL serum (reflects <1% of total body magnesium, an imperfect status marker; some functional practitioners argue RBC magnesium is more informative, though it's not a routinely available thyroid-panel test).

Food first: Leafy greens, nuts, seeds, legumes, whole grains, dark chocolate; magnesium glycinate or citrate are generally better absorbed/tolerated than oxide for supplementation.

When to see someone: High-dose magnesium supplements cause diarrhea before serious harm in people with normal kidney function, but anyone with reduced kidney function (low eGFR) needs medical guidance before supplementing, since magnesium is renally cleared. Magnesium (like calcium and iron) can also block levothyroxine absorption if taken too close together -- see Medication Interactions below.