What is the optimal TSH level?

The optimal TSH range is 1.0-2.5 mIU/L, narrower than the standard lab range of 0.5-4.5. The American Association of Clinical Endocrinologists advocated for narrowing the range to 0.3-3.0 in 2002. TSH above 2.5 with symptoms warrants investigation of free T3, free T4, reverse T3, and TPO antibodies.

What is reverse T3 and why does it matter?

Reverse T3 (rT3) is an inactive isomer of T3 that blocks thyroid hormone receptors without activating them. It is produced in excess during chronic stress, severe illness, and selenium deficiency. Elevated rT3 with normal TSH and T4 but low free T3 is a real clinical pattern that produces every symptom of hypothyroidism. The free T3-to-rT3 ratio below 20 suggests significant rT3 interference.

Does selenium help thyroid function?

Yes. Selenium is a cofactor for the deiodinase enzymes that convert T4 to active T3. Selenium deficiency impairs this conversion and increases reverse T3 production. A 2002 meta-analysis found selenium supplementation (200 mcg selenomethionine daily) reduced TPO antibody titers by 40-50% in Hashimoto's patients. 1-2 Brazil nuts daily provide 100-200 mcg of selenium naturally.

What is Hashimoto's thyroiditis?

Hashimoto's thyroiditis is autoimmune destruction of the thyroid gland, the most common cause of hypothyroidism in the Western world, affecting up to 14% of the population. Elevated TPO antibodies (above 35 IU/mL) confirm Hashimoto's even with normal TSH. The autoimmune trigger involves gut permeability, molecular mimicry with gluten, iodine excess, and selenium deficiency.

Thyroid Function & TSH Testing for Hypothyroidism

Quick answer: Hypothyroidism affects 20 million Americans, but the standard TSH-only test misses most cases of functional hypothyroidism. You can have a TSH in the “normal” range of 0.5–4.5 mIU/L while your free T3 (the active thyroid hormone) is in the lower third of the reference range — a pattern that produces every symptom of hypothyroidism. The labs that actually matter are TSH, free T3, free T4, reverse T3, and TPO antibodies — and most physicians only order the first one.

Thyroid function testing and hypothyroidism symptoms Dr. Tom Biernacki

The thyroid is the most over-simplified organ in medicine. Endocrinologists will tell you that TSH is the “gold standard” test and that a value within the reference range means your thyroid is fine. What they will less often tell you is that the TSH reference range (0.5–4.5 mIU/L in most labs) includes symptomatic individuals in the upper quartile, that subclinical hypothyroidism (TSH 2.5–4.5) is associated with significantly elevated cardiovascular risk and cognitive decline, and that the conversion of T4 to T3 — the active thyroid hormone — can be impaired even with a normal TSH and normal T4.

I see two distinct thyroid problem patterns clinically: patients who are on levothyroxine (T4-only treatment) but still feel terrible because their T4-to-T3 conversion is impaired, and patients who have been told their labs are “normal” but have every symptom of hypothyroidism because their free T3 is in the bottom 25% of the reference range. Both groups are failed by the TSH-only testing paradigm.

Here is what you need to know about thyroid function, the correct tests, and the interventions that support optimal thyroid health. Welcome to The Private Practice. I am Dr. Tom.

How the Thyroid Works: The Basics You Need to Know

The thyroid gland produces two hormones: T4 (thyroxine, 80% of thyroid output) and T3 (triiodothyronine, 20% of direct output). T4 is largely a prohormone — it must be converted to T3 by deiodinase enzymes (primarily in the liver, kidney, gut, and muscle) to become biologically active. T3 is the hormone that actually enters cells and binds thyroid hormone receptors to drive metabolism, thermogenesis, protein synthesis, and neurological function.

TSH (thyroid-stimulating hormone), produced by the pituitary, is the master regulator. When T3 levels fall, the pituitary increases TSH to stimulate the thyroid to produce more T4 and T3. When T3 is adequate, TSH falls. This negative feedback loop is the basis for the TSH test — but the loop only tells you what the pituitary thinks, not what is actually happening at the tissue level where T4-to-T3 conversion occurs.

Why TSH Alone Is Insufficient

The TSH test is a pituitary output test, not a tissue thyroid hormone test. Three critical points:

TSH can be normal while free T3 is low if T4-to-T3 conversion is impaired. The pituitary receives adequate T4 feedback and doesn’t raise TSH, but peripheral tissues are not getting enough T3.
The TSH reference range upper limit of 4.5 mIU/L is controversial. The American Association of Clinical Endocrinologists advocated in 2002 for a narrowed range of 0.3–3.0 mIU/L, and multiple studies show that TSH above 2.5 is associated with higher rates of Hashimoto’s antibody development, impaired lipid profiles, and cognitive symptoms.
Reverse T3 (rT3) — an inactive isomer of T3 that blocks T3 receptors without activating them — is produced in excess during chronic stress, severe illness, nutrient deficiency, and caloric restriction. Normal TSH and T4 with elevated rT3 and low free T3 is a real and under-diagnosed clinical pattern.

The Complete Thyroid Panel

The tests I recommend ordering, as part of the comprehensive panel discussed in how to read blood test results:

TSH

Optimal range: 1.0–2.5 mIU/L (not the lab standard 0.5–4.5). TSH above 2.5 with symptoms warrants investigation. TSH below 0.5 with fatigue raises concern for hyperthyroidism or iodine excess. TSH above 4.5 is overt hypothyroidism by any standard and requires treatment in symptomatic patients.

Free T4 and Free T3

Free T4 reflects thyroid gland output (and is what levothyroxine supplements). Free T3 reflects the active hormone available to tissues. The key ratio: free T3 should be in the upper half of its reference range. Free T3 in the lower third of the reference range (typically below 2.8–3.0 pg/mL) consistently produces hypothyroid symptoms even with normal TSH and normal free T4. This is functional hypothyroidism via impaired conversion, and it is one of the most common missed diagnoses I encounter.

Reverse T3 (rT3)

Reverse T3 is elevated by chronic stress (elevated cortisol directly increases rT3 production — the cortisol connection is significant), caloric restriction, prolonged illness, and selenium deficiency. The free T3-to-rT3 ratio is a useful functional marker: below 20 (with free T3 in pg/mL and rT3 in pg/mL) suggests clinically significant rT3 interference with thyroid hormone action. Elevated rT3 is the “emergency brake” of thyroid metabolism — the body slows metabolism under perceived threat conditions, regardless of what the TSH shows.

TPO Antibodies and Anti-Thyroglobulin Antibodies

Hashimoto’s thyroiditis — autoimmune destruction of the thyroid — is the most common cause of hypothyroidism in the Western world, affecting up to 14% of the population. Elevated TPO antibodies (above 35 IU/mL) with normal TSH indicate Hashimoto’s in an early or compensated stage. Many physicians will not treat elevated antibodies with normal TSH, but the evidence supports that elevated antibodies with any symptoms — even with “normal” TSH — warrant attention to the underlying autoimmune trigger (gluten sensitivity, gut dysbiosis, iodine excess, selenium deficiency). See gut health and the microbiome for the gut-thyroid autoimmunity connection.

Symptoms of Suboptimal Thyroid Function

The classic symptoms of hypothyroidism — fatigue, cold intolerance, weight gain, constipation, brain fog, dry skin, hair loss, depression — also appear at the subclinical level (TSH 2.5–4.5) and in functional hypothyroidism (normal TSH with low free T3). The most consistent early markers in my clinical experience:

Fatigue disproportionate to activity — particularly morning fatigue that does not improve with more sleep
Cold hands and feet and intolerance to cold environments (low T3 = impaired thermogenesis)
Hair loss or thinning — particularly outer third of the eyebrows (a classic hypothyroid sign)
Constipation — thyroid hormone drives gastrointestinal motility; low T3 slows it
Elevated LDL and total cholesterol — thyroid hormone upregulates LDL receptor expression; hypothyroidism produces a secondary dyslipidemia. An unexplained rise in LDL should prompt thyroid testing alongside the lipid workup discussed in what your lipid panel isn’t telling you.
Slow reflexes and bradycardia — both are driven by inadequate T3 at the tissue level
Depression and cognitive slowing — T3 receptors are densely expressed in the hippocampus and prefrontal cortex; functional hypothyroidism is one of the most common reversible causes of depression and should be excluded before psychiatric medication

The Nutritional Drivers of Thyroid Dysfunction

Selenium: The Most Important Thyroid Mineral You Are Not Getting

Selenium is the cofactor for the deiodinase enzymes (types 1, 2, and 3) that convert T4 to T3 and inactivate T3. The thyroid gland has the highest selenium content per gram of any tissue in the body. Selenium deficiency impairs T4-to-T3 conversion and increases rT3 production. It also impairs glutathione peroxidase activity in thyroid tissue, increasing oxidative damage — a contributor to Hashimoto’s pathogenesis. A 2002 meta-analysis in the European Journal of Endocrinology found that selenium supplementation (200 mcg daily as selenomethionine) reduced TPO antibody titers by 40–50% in Hashimoto’s patients. The Brazil nut connection is real: 1–2 Brazil nuts daily provide approximately 100–200 mcg of selenium. The supplement form: selenomethionine (organic, better absorbed) at 100–200 mcg daily.

Iodine: Necessary but Easily Overdone

Iodine is the primary substrate for thyroid hormone synthesis (T4 = four iodine atoms, T3 = three). Iodine deficiency was the most common cause of hypothyroidism globally before iodized salt programs. However, excessive iodine intake triggers the Wolff-Chaikoff effect — a transient suppression of thyroid hormone synthesis — and in genetically susceptible individuals with latent Hashimoto’s, iodine excess can precipitate or worsen autoimmune thyroid disease. The therapeutic window is narrow: 150–250 mcg daily is optimal; megadose iodine supplementation (3–50 mg, as promoted in some alternative medicine circles) is potentially harmful for the 14% of the population with subclinical Hashimoto’s.

Magnesium, Zinc, and Iron

Thyroid peroxidase — the enzyme that incorporates iodine into tyrosine to make T4 and T3 — requires iron as a cofactor. Iron deficiency reduces thyroid hormone synthesis independently of iodine status. Zinc is required for TSH receptor signaling and for TRH (thyrotropin-releasing hormone) production in the hypothalamus. Magnesium is involved in thyroid hormone transport and cellular T3 receptor activation. All three of these deficiencies are common, underappreciated contributors to functional hypothyroidism — and all three are addressed in my posts on magnesium deficiency and the broader lab testing guide.

Chronic Stress, Cortisol, and the Thyroid Axis

Cortisol is the most potent known suppressor of T4-to-T3 conversion. Elevated cortisol increases type 3 deiodinase activity (which converts T4 to rT3 rather than active T3) and suppresses the hypothalamic TRH pulse that drives TSH and thyroid hormone production. This is the mechanism behind the rT3 elevation seen in chronically stressed patients with “normal” thyroid panels. A patient with high-normal TSH, normal T4, low-normal free T3, and elevated rT3 in the context of chronic stress has a thyroid problem that will not respond to thyroid medication alone — the cortisol driver must be addressed. See what chronic stress is doing to your body for the full HPA axis picture.

Treatment Options and When Medication Is Appropriate

Levothyroxine (T4-Only): The Standard of Care and Its Limitations

Levothyroxine (synthetic T4) is the first-line treatment for hypothyroidism in all major endocrinology guidelines. It is effective for patients who convert T4 to T3 normally. The problem: approximately 15–20% of patients on adequate levothyroxine (normalized TSH) continue to have persistent hypothyroid symptoms. These are patients with impaired T4-to-T3 conversion — a pattern that does not respond to T4-only treatment regardless of dose optimization.

Combination T4+T3 Therapy

Liothyronine (synthetic T3, brand name Cytomel) added to levothyroxine — or natural desiccated thyroid (NDT, which contains both T4 and T3 in the physiological 4:1 ratio) — addresses the conversion deficit. A 2019 meta-analysis in Thyroid found that a subset of hypothyroid patients significantly prefer combination T4+T3 therapy and show improved cognitive function, mood, and quality of life compared to T4 monotherapy. This remains controversial among endocrinologists, but the evidence is sufficient to warrant a trial in patients who have failed T4-only treatment with persistent symptoms and low free T3.

Frequently Asked Questions

Can I have hypothyroidism with a normal TSH?

Yes — in two ways. First, functional hypothyroidism: normal TSH with low free T3 due to impaired T4-to-T3 conversion (from cortisol, selenium deficiency, or inflammation). Second, early Hashimoto’s: normal TSH with elevated TPO antibodies and progressive thyroid tissue destruction — TSH will not rise until significant gland destruction has occurred. Both patterns produce hypothyroid symptoms and both are missed by TSH-only testing.

What foods should I avoid with hypothyroidism?

Raw goitrogenic vegetables (broccoli, kale, cabbage, Brussels sprouts) contain isothiocyanates that inhibit thyroid peroxidase in large quantities — but cooking inactivates most of this activity, and normal servings of cooked cruciferous vegetables are not a clinically meaningful concern for most patients. The more important dietary interventions: avoid iodine excess (kelp supplements, excessive seaweed), address gluten sensitivity in Hashimoto’s patients (gluten molecular mimicry with thyroid peroxidase has been documented in multiple studies), and ensure adequate selenium and zinc intake.

Does Hashimoto’s require a gluten-free diet?

The association between celiac disease and Hashimoto’s thyroiditis is well-established: celiac affects 4–6% of Hashimoto’s patients (vs. 1% of the general population), and strict gluten elimination has been shown to reduce TPO antibody titers in celiac-positive Hashimoto’s patients. For Hashimoto’s patients without celiac, the evidence for strict gluten avoidance is weaker but the theoretical basis is reasonable (molecular mimicry, intestinal permeability). A supervised 90-day gluten elimination trial is worth considering in any patient with Hashimoto’s and persistent symptoms despite medication.

Does low thyroid function cause weight gain?

Yes — but the effect is often overestimated. The average weight gain from overt hypothyroidism is 5–10 lbs, mostly from fluid retention (myxedema) and reduced basal metabolic rate. Reversing hypothyroidism rarely produces dramatic weight loss unless the obesity was primarily thyroid-driven. The metabolic weight gain that most patients attribute to their thyroid is more often driven by the insulin resistance that frequently co-exists with hypothyroidism — see insulin resistance: why 40% of adults have it and don’t know it for the overlap and clinical picture.

What is the connection between sleep and thyroid function?

TSH has a strong circadian rhythm, peaking at night (around midnight to 4 AM) and reaching its nadir in the afternoon. Sleep deprivation — particularly disruption of the nocturnal TSH peak — reduces thyroid hormone synthesis and lowers T3 levels measurably within days. This is one mechanism by which chronic poor sleep produces fatigue that mimics hypothyroidism. The overlap with cortisol-driven sleep disruption is significant: both conditions suppress the HPT (hypothalamic-pituitary-thyroid) axis, and both are addressed in why cortisol prevents you from sleeping.

The Bottom Line

The TSH-only approach to thyroid testing leaves a substantial proportion of symptomatic patients undiagnosed and untreated. The complete panel — TSH, free T3, free T4, reverse T3, and TPO antibodies — gives you an actionable picture. The key targets: TSH 1.0–2.5, free T3 in the upper half of the reference range, minimal rT3 elevation, and negative TPO antibodies.

The nutritional and lifestyle interventions with the strongest evidence: selenium (200 mcg selenomethionine daily), adequate zinc and magnesium, cortisol management (the single most impactful thyroid intervention that does not involve medication), and gluten elimination in confirmed Hashimoto’s patients. These address the upstream causes rather than just suppressing the downstream TSH signal.

I test all of this on myself first. That is the honest truth.

For comprehensive thyroid panel interpretation and protocol design, reach me at health-consultation or see the course library at health-courses.

Thyroid Function: Why Your TSH Is Normal But You Still Feel Terrible