Complete Thyroid Panel: What Your Doctor Isn’t Testing

The TSH Deception

Here is the most consequential lie in modern medicine: that TSH alone tells you whether your thyroid is healthy. Millions of patients sit in doctor’s offices, drowning in fatigue, brain fog, hair loss, weight gain, depression, and cold hands, and they are told, “Your thyroid is fine — your TSH is normal.”

TSH is not a thyroid hormone. It is a pituitary hormone. It is a request sent from the brain to the thyroid, asking for more hormone. Testing only TSH to assess thyroid function is like judging a restaurant’s food quality by reading the customer’s order slip. You have no idea what was actually delivered to the table.

A complete thyroid evaluation requires seven to nine markers. Most doctors order one. This gap leaves an estimated 60% of thyroid dysfunction undiagnosed.

The Complete Thyroid Panel

TSH (Thyroid Stimulating Hormone)

Optimal: 1.0-2.0 mIU/L (standard range 0.5-4.5)

The standard range of 0.5-4.5 is absurdly wide. A TSH of 4.0 is “normal” by lab criteria, but the research is clear: TSH above 2.5 is associated with increased risk of progression to overt hypothyroidism, elevated cholesterol, and cardiovascular disease. The NHANES III study found that 95% of people without thyroid disease have a TSH between 0.4 and 2.5.

TSH also follows a circadian rhythm — highest in early morning (around 2-4 AM), lowest in afternoon. A TSH drawn at 4 PM may look normal when a morning draw would have been elevated. Always test in the morning, fasting (eating suppresses TSH).

But here is the deeper problem: TSH can be suppressed or blunted by cortisol, inflammation, dopamine, somatostatin, and metformin. A “normal” TSH in a chronically stressed patient may be a falsely normal TSH.

Free T4 (Thyroxine)

Optimal: 1.1-1.5 ng/dL

Free T4 is the unbound, bioavailable form of thyroxine — the hormone the thyroid gland produces most abundantly. Total T4 is largely useless because it includes protein-bound hormone (bound to thyroxine-binding globulin, albumin, and transthyretin). Estrogen, pregnancy, oral contraceptives, and liver disease all alter binding protein levels, making total T4 unreliable.

T4 is the storage form — the prohormone. It must be converted to T3 to become active. Think of T4 as crude oil. It has potential energy, but it cannot power anything until it is refined into gasoline (T3).

Free T3 (Triiodothyronine)

Optimal: 3.0-4.0 pg/mL

This is the active thyroid hormone — the one that enters cells, binds nuclear receptors, and drives metabolism, body temperature, heart rate, cognitive function, mood, hair growth, and gut motility. Free T3 is the single most important thyroid marker that most doctors never order.

You can have a perfectly normal TSH and Free T4 while Free T3 is in the basement. This happens because the conversion of T4 to T3 occurs primarily in the liver (60%), gut (20%), and peripheral tissues — not the thyroid gland. If your liver is sluggish, your gut is inflamed, or you are chronically stressed, conversion fails. The pituitary sees adequate T4 and keeps TSH normal, but your cells are hypothyroid.

This is cellular hypothyroidism — and it is invisible to a standard TSH test.

Reverse T3 (rT3)

Optimal: <15 ng/dL (standard range 9.2-24.1)

Reverse T3 is the anti-thyroid hormone — the brake pedal. It is structurally similar to T3 but binds thyroid receptors without activating them, effectively blocking T3 from doing its job. The body produces rT3 intentionally during times of physiological conservation: acute illness, starvation, severe stress, surgery, or trauma. It is a survival mechanism — slow metabolism to conserve energy during crisis.

The problem arises when rT3 stays chronically elevated: chronic stress (high cortisol drives T4 toward rT3 instead of T3), chronic inflammation, caloric restriction and crash dieting, iron deficiency, selenium deficiency, liver dysfunction, chronic illness, and certain medications (beta-blockers, amiodarone, high-dose corticosteroids).

Free T3 to Reverse T3 Ratio

Optimal: >0.2 (calculate as Free T3 in pg/mL divided by Reverse T3 in ng/dL)

This ratio is the best single marker of thyroid function at the cellular level. It represents the gas-to-brake ratio. A patient can have a “normal” TSH of 2.0, a normal Free T4 of 1.2, a borderline Free T3 of 2.5, and a Reverse T3 of 22 — giving a ratio of 0.11. That patient is functionally hypothyroid at the tissue level despite a “normal” panel by conventional standards.

When the ratio is below 0.2, focus shifts to identifying and correcting the driver: stress management, anti-inflammatory protocol, iron repletion, selenium supplementation, liver support, and caloric adequacy.

Thyroid Antibodies: Catching Autoimmunity Early

TPO Antibodies (Anti-thyroid peroxidase): <2 IU/mL (standard “normal” <34) Thyroglobulin Antibodies (Anti-Tg): <2 IU/mL (standard “normal” <40)

The standard thresholds are dangerously permissive. A TPO of 30 is called “normal.” It is not. Any detectable elevation of thyroid antibodies indicates the immune system is attacking the thyroid gland — this is Hashimoto’s thyroiditis, the most common autoimmune disease in the world.

Here is the critical timeline most doctors miss: thyroid antibodies rise 5-10 years before TSH becomes abnormal. During this silent autoimmune phase, the thyroid is being destroyed, but it compensates by working harder. TSH stays normal. Symptoms accumulate. The patient is dismissed. By the time TSH finally rises, 70-80% of the thyroid gland may be damaged.

Testing antibodies allows early intervention — removing dietary triggers (gluten is the most researched; molecular mimicry between gliadin and thyroid peroxidase), supporting immune regulation (vitamin D, selenium, omega-3), healing the gut (the epicenter of autoimmune initiation), and reducing inflammation.

Thyroglobulin itself (not the antibody) serves as a tumor marker in patients who have had thyroidectomy for thyroid cancer — it should be undetectable post-surgery. Rising thyroglobulin suggests recurrence.

T3 Uptake (T3RU) measures the binding capacity of thyroid-binding proteins. It moves inversely with TBG levels. When TBG is high (estrogen, pregnancy, liver disease), T3 uptake is low. Used to calculate the Free Thyroxine Index (FTI = T4 x T3RU).

Pattern Recognition: Reading the Story

Primary Hypothyroidism

TSH high + FT4 low + FT3 low. The thyroid gland itself is failing. Most common cause: Hashimoto’s. Check antibodies.

Cellular Hypothyroidism (Euthyroid Sick Syndrome / Low T3 Syndrome)

TSH normal + FT4 normal or low-normal + FT3 low + RT3 high. The TSH lies because the pituitary is getting enough T4, but peripheral tissues cannot convert it to active T3. This pattern is rampant in chronic stress, chronic dieters, and patients with chronic inflammatory conditions. It will be missed by every doctor who only checks TSH.

Subclinical Hypothyroidism

TSH 2.5-10 + FT4 normal + FT3 often low-normal. The “gray zone” that conventional medicine watches and waits on. Functional medicine treats — especially if antibodies are present, symptoms are significant, or cholesterol is rising.

Hyperthyroidism (Graves’ Disease)

TSH low (<0.1) + FT4 high + FT3 high + TSI (thyroid stimulating immunoglobulin) positive. An autoimmune condition where antibodies stimulate the thyroid to overproduce.

Early Hashimoto’s

TSH normal + FT4 normal + FT3 normal + TPO/TG antibodies elevated. The thyroid is under attack but still compensating. This is the golden window for intervention. Remove the triggers, support the immune system, protect the gland.

Conversion Problem

TSH normal or slightly elevated + FT4 adequate + FT3 low + RT3 high. The raw material (T4) is there but the refinery is broken. Address the conversion blockers.

Nutrients That Drive Thyroid Conversion

Selenium (200-400 mcg/day as selenomethionine): The T4-to-T3 conversion enzyme (5’-deiodinase) is a selenoprotein. Selenium is also required for glutathione peroxidase, which protects the thyroid from hydrogen peroxide damage during hormone synthesis. Clinical trials show selenium reduces TPO antibodies by 40-60% in Hashimoto’s patients (Turker et al., 2006; Mazokopakis et al., 2007).

Zinc (30 mg/day as zinc picolinate or bisglycinate): Required for T3 binding to its nuclear receptor. Zinc deficiency impairs both thyroid hormone synthesis and T4-to-T3 conversion. Low zinc also blunts TSH response — another reason TSH can appear falsely normal.

Iron (ferritin target 70-90 ng/mL): Thyroid peroxidase (TPO) is an iron-dependent enzyme. Without adequate iron, the thyroid cannot produce T4 in the first place. Low ferritin is one of the most common and overlooked causes of persistent hypothyroid symptoms despite medication.

Iodine (150-300 mcg/day — use with extreme caution in Hashimoto’s): Iodine is the raw material for thyroid hormone (T4 has 4 iodine atoms, T3 has 3). Deficiency causes goiter and hypothyroidism. However, excess iodine in Hashimoto’s patients can worsen autoimmune flare by increasing hydrogen peroxide production in the thyroid. Always ensure selenium status is adequate before iodine supplementation.

Vitamin D (target 50-70 ng/mL): Vitamin D receptors are present on thyroid cells and immune cells. Vitamin D deficiency is strongly associated with Hashimoto’s. Supplementation (4000-5000 IU/day) has been shown to reduce TPO antibodies.

Vitamin A (retinol, not beta-carotene): Vitamin A is required for TSH receptor function and thyroid hormone signaling. Hypothyroid patients often have impaired conversion of beta-carotene to retinol (the enzyme requires thyroid hormone), creating a vicious cycle.

Cortisol status: Cortisol and thyroid hormone are intimately linked. High cortisol pushes T4 toward Reverse T3. Low cortisol (adrenal insufficiency) impairs thyroid hormone action at the cellular level — cells need cortisol to properly respond to T3. This is why the functional medicine rule is: always assess and support adrenals before or alongside thyroid treatment. Starting thyroid medication in an adrenally depleted patient can cause worsening symptoms because you are accelerating a metabolism that has no fuel.

Medication Monitoring

Levothyroxine (T4 only — Synthroid, Levoxyl, Tirosint): Test TSH + FT4 + FT3 six weeks after dose change. Take medication on empty stomach, 30-60 minutes before food. Separate from calcium, iron, and coffee by 4 hours. Many patients have adequate FT4 but low FT3 on levothyroxine alone — they are poor converters and may benefit from combination therapy.

Natural Desiccated Thyroid (NDT — Armour, NP Thyroid, WP Thyroid): Contains both T4 and T3 in a fixed ratio (~4:1). FT3 will peak 2-4 hours after dosing and may appear falsely elevated. Draw blood before morning dose or at consistent timing. NDT provides a more physiologic hormone profile for many patients.

Liothyronine (T3 only — Cytomel): Short half-life (2.5 hours vs T4’s 7 days). Draw blood before dose. Consider sustained-release compounded T3 for smoother levels.

Thyroid Connections to Other Systems

Thyroid-Gut Axis: 20% of T4-to-T3 conversion occurs in the gut, mediated by intestinal sulfatase and bacterial beta-glucuronidase. Dysbiosis directly impairs thyroid hormone activation. Furthermore, intestinal permeability (leaky gut) is a prerequisite for autoimmune thyroid disease — molecular mimicry requires intact antigens crossing an impaired gut barrier.

Thyroid-Adrenal Connection: Hypothyroidism slows cortisol clearance (raising cortisol), while adrenal dysfunction impairs T4-to-T3 conversion and thyroid receptor sensitivity. The two systems must be addressed together. Clinically, treat adrenals first.

Thyroid-Iron Link: Iron deficiency impairs thyroid hormone synthesis (TPO is iron-dependent), impairs T4-to-T3 conversion, and blunts TSH response. A ferritin below 70 makes it nearly impossible to optimize thyroid function.

Thyroid-Sex Hormone Link: Estrogen increases thyroxine-binding globulin (TBG), reducing free T4 availability. This is why hypothyroid symptoms often emerge or worsen during pregnancy, oral contraceptive use, or perimenopause. Conversely, hypothyroidism elevates SHBG, disrupting testosterone and estrogen balance, contributing to menstrual irregularities and low libido.

The thyroid does not operate in isolation. It is a node in a network. Treating the thyroid without addressing the gut, adrenals, iron, and sex hormones is treating a symptom while ignoring the system.