Thyroid Function Tests (TFT): Understanding Your Blood Test Series

1. Overview: What this panel reveals and why it is important

The thyroid function test panel is not a single hormone assay but a hierarchical interrogation of the hypothalamic‑pituitary‑thyroid (HPT) axis. It simultaneously assesses the secretory output of the thyroid gland (thyroxine – T4; triiodothyronine – T3) and the integrity of the central feedback loop (thyroid‑stimulating hormone – TSH).

The clinical power of TFTs lies in pattern recognition across the axis. An elevated TSH with low free T4 unequivocally identifies primary hypothyroidism. A suppressed TSH with elevated free T4 signals primary hyperthyroidism. A low free T4 with normal or low TSH points to central (pituitary/hypothalamic) hypothyroidism—a critically different diagnosis. Normal TSH with isolated low T3 suggests euthyroid sick syndrome, not thyroid disease.

No single test is interpreted in isolation. TSH is the most sensitive marker of thyroid status, but it is blind to central hypothyroidism, resistant to rapid fluctuations, and susceptible to assay interference. Free T4 confirms the diagnosis and guides severity. Free T3 informs tissue thyrotoxicosis, particularly in T3‑toxicosis and central hyperthyroidism. Thyroid antibodies (TPO, Tg, TRAb) establish aetiology—autoimmune, destructive, or stimulatory.

Thus, the TFT panel is a conversation between the pituitary and the thyroid. Listen to the TSH. Confirm with free T4. Refine with free T3 and antibodies. Treat the axis, not the individual number.

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2. What does it measure

A standard TFT panel includes the following components. Reference ranges are laboratory‑ and method‑specific; values below are approximate adult ranges.

Primary screening and feedback marker:

· Thyroid‑stimulating hormone (TSH): 0.4–4.5 mIU/L (some labs: 0.5–5.0). Pituitary glycoprotein; inverse log‑linear relationship with circulating thyroid hormone. Most sensitive index of thyroid status.

Peripheral hormone concentrations:

· Free thyroxine (FT4): 0.8–1.8 ng/dL (9–23 pmol/L). Unbound, biologically active fraction. Reflects thyroid gland secretion.

· Free triiodothyronine (FT3): 2.3–4.2 pg/mL (3.5–6.5 pmol/L). Predominantly derived from peripheral deiodination of T4. More potent, shorter half‑life.

· Total T4 / Total T3: Measure bound + free fraction; influenced by binding proteins (thyroxine‑binding globulin, albumin). Less commonly used; free hormone assays preferred.

Aetiological markers (autoimmunity, stimulation):

· Thyroid peroxidase antibody (TPOAb): Positive in Hashimoto’s thyroiditis (90–95%) and Graves’ disease (50–80%). Marker of autoimmune destruction.

· Thyroglobulin antibody (TgAb): Less specific; may be positive in Hashimoto’s, Graves’, and some healthy individuals. Interferes with thyroglobulin measurement in thyroid cancer follow‑up.

· TSH receptor antibody (TRAb): Subtypes: stimulating (TSI) – causative in Graves’ disease; blocking – may cause hypothyroidism. Essential for diagnosing Graves’ and predicting neonatal thyrotoxicosis.

Additional/ancillary tests:

· Reverse T3 (rT3): Biologically inactive; elevated in euthyroid sick syndrome, certain drugs. Not part of routine panel.

· Thyroglobulin (Tg): Tumour marker for differentiated thyroid cancer; not for general thyroid function assessment.

· Calcitonin: Medullary thyroid cancer; not part of routine TFT.

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3. Other factors connected to this panel

Preanalytical and biological variables:

· Circadian rhythm: TSH peaks in the early morning (02:00–04:00), nadir in afternoon. Single non‑fasting sample adequate; serial measurements should be same time of day.

· Acute illness / hospitalisation: Suppresses TSH, lowers T3 (euthyroid sick syndrome); do not test thyroid function during acute non‑thyroidal illness unless strong suspicion.

· Pregnancy:

· hCG stimulates TSH receptor (weakly); first trimester TSH often low (0.1–0.4 mIU/L).

· TBG rises (oestrogen effect); total T4/T3 increase, free hormone assays by equilibrium dialysis preferred; automated immunoassays may be artefactually low.

· Trimester‑specific TSH reference ranges: first 0.1–2.5, second 0.2–3.0, third 0.3–3.0 mIU/L (approximate).

· Age: TSH mildly increases with age (>70 years); upper limit may be 5.5–6.5 mIU/L in healthy elderly.

· Ethnicity: Black populations have slightly lower TSH, higher T4; Caucasian/Asian have higher TSH.

· Body mass index: Positive correlation with TSH (within normal range); obesity associated with mild TSH elevation (2.5–5.0).

· Smoking: Thiocyanates in smoke inhibit iodine uptake, increase thyroid autoimmunity risk; not recommended.

· Iodine intake: Chronic deficiency → goitre, normal/low TSH; acute excess (contrast, amiodarone) → transient hypo‑ or hyperthyroidism (Jod‑Basedow phenomenon).

Medications affecting TFTs:

Affect TSH secretion (central):

· Dopamine, dobutamine: Suppress TSH (central hypothyroidism pattern).

· Glucocorticoids: Suppress TSH, inhibit T4→T3 conversion.

· Octreotide: Suppresses TSH.

· Metformin: May lower TSH in euthyroid individuals with diabetes.

Affect thyroid hormone synthesis/release:

· Amiodarone: Type 1 (iodine‑induced hyperthyroidism), Type 2 (destructive thyroiditis), or hypothyroidism; complex effects.

· Lithium: Inhibits thyroid hormone release; causes hypothyroidism (10–20%).

· Thionamides (methimazole, PTU): Inhibit thyroid peroxidase; used to treat hyperthyroidism.

· Iodine, iodinated contrast: Inhibit organification (Wolff‑Chaikoff effect).

Affect binding proteins:

· Oestrogens (oral contraceptives, HRT): Increase TBG → increase total T4/T3; free hormones usually normal. TSH unaffected.

· Androgens, anabolic steroids: Decrease TBG → low total T4/T3; free normal.

· Phenytoin, carbamazepine: Displace T4 from binding proteins, increase metabolism; often low total and free T4, normal TSH.

Affect peripheral deiodination (T4→T3):

· Amiodarone, glucocorticoids, propranolol (high dose), iodinated contrast: Inhibit type 1 5'‑deiodinase → low T3, high reverse T3, normal TSH.

Interfere with laboratory assays:

· Biotin (vitamin B7): Widely used in hair, skin, nail supplements; causes falsely high FT4/FT3 and falsely low TSH on streptavidin‑biotin immunoassays. Must stop biotin ≥48 hours (longer if mega‑doses) before TFT.

· Heterophile antibodies / macro‑TSH: Falsely high TSH (TSH bound to immunoglobulin); suspect when TSH elevated but FT4 normal, no symptoms. Check with heterophile blocking tube, PEG precipitation.

· Anti‑streptavidin antibodies: Can also interfere.

Physiological and demographic factors:

· Neonates: TSH surge at birth (up to 20–30 mIU/L), falls by day 3–5.

· Pregnancy: As above.

· Fasting / malnutrition: Low T3, normal TSH, normal T4 (euthyroid sick variant).

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4. Disorders related to abnormal values: Pattern recognition

The TFT panel is interpreted using a stepwise, hierarchical algorithm. TSH is the first discriminant. If TSH abnormal, proceed to FT4, FT3, antibodies.

a. Primary hypothyroidism pattern

Laboratory profile:

· TSH ↑ (usually >4.5–5.0 mIU/L)

· FT4 ↓ (confirmatory)

· FT3 may be low or normal (preferential T3 preservation)

· TPOAb/TgAb often positive (autoimmune aetiology)

Differential diagnosis:

· Chronic autoimmune thyroiditis (Hashimoto’s): Most common cause; positive TPOAb; firm, rubbery goitre (may be atrophic).

· Post‑ablative: Radioiodine therapy, thyroidectomy, external radiation.

· Iatrogenic: Antithyroid drugs (over‑treatment), lithium, amiodarone, tyrosine kinase inhibitors.

· Iodine deficiency or excess: Endemic cretinism (deficiency); iodine excess (contrast, amiodarone) can induce hypothyroidism.

· Infiltrative: Riedel thyroiditis, sarcoidosis, amyloidosis.

· Transient: Subacute thyroiditis (painful), painless/postpartum thyroiditis – usually hyperthyroid phase first, then transient hypothyroidism.

Outlier scenarios:

· TSH >100 mIU/L with minimal symptoms: Chronic, slowly progressive autoimmune hypothyroidism.

· TSH elevated, FT4 low, no antibodies, no goitre, no prior ablation: Consider iodine deficiency/excess, drugs, or rare genetic causes (TSH resistance).

· TSH elevated, FT4 low, positive TPOAb, postpartum: Postpartum thyroiditis (usually resolves in 6–12 months).

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b. Subclinical hypothyroidism pattern

Laboratory profile:

· TSH ↑ (usually 4.5–10 mIU/L; >10 often considered overt)

· FT4 normal

· FT3 normal

· TPOAb may be positive or negative

Differential diagnosis:

· Mild autoimmune thyroiditis: TPOAb positive; progress to overt hypothyroidism at 2–5% per year.

· Recovery phase of thyroiditis: After subacute, painless, postpartum.

· Medication effect: Lithium, amiodarone (early), inadequate levothyroxine dose.

· Obesity: Mild TSH elevation (2.5–5.0) without FT4 abnormality; not true hypothyroidism.

· Assay interference: Macro‑TSH (heterophile antibodies) – TSH elevated but FT4 normal, no symptoms.

Outlier scenarios:

· TSH 5–10, TPOAb positive, young, pregnant or planning pregnancy: Treat with levothyroxine (reduce risk of progression, pregnancy complications).

· TSH 5–10, TPOAb negative, elderly (>70): Often observe; treatment does not improve symptoms or cardiovascular outcomes.

· TSH 5–10, FT4 normal, symptoms of hypothyroidism: Controversial; may trial levothyroxine for 3–6 months.

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c. Primary hyperthyroidism pattern

Laboratory profile:

· TSH ↓ (usually <0.1 mIU/L)

· FT4 ↑ or FT3 ↑ (or both)

· FT3 may be disproportionately elevated in Graves’ or T3‑toxicosis

Differential diagnosis:

· Graves’ disease: Diffuse goitre, orbitopathy, dermopathy; TRAb positive (stimulating); TPOAb often positive.

· Toxic multinodular goitre (Plummer disease): Older adults; gradual onset; TRAb negative.

· Solitary toxic adenoma: Hot nodule on scintigraphy; TSH suppressed, FT4/FT3 elevated.

· Thyroiditis (destructive): Subacute (painful, viral prodrome), painless, postpartum, amiodarone‑induced (type 2), radiation thyroiditis. Transient release of stored hormone; low RAIU.

· Iatrogenic / factitious: Excessive levothyroxine; low Tg, low RAIU.

· Excess iodine (Jod‑Basedow): Iodinated contrast, amiodarone (type 1) – especially in nodular goitre.

Outlier scenarios:

· TSH suppressed, FT4 normal, FT3 elevated: T3‑toxicosis (Graves’ or toxic nodule). Check FT3.

· TSH suppressed, FT4/FT3 elevated, TRAb negative, no goitre: Consider painless thyroiditis, amiodarone, or factitious.

· TSH suppressed, FT4 elevated, TRAb negative, low RAIU: Destructive thyroiditis; supportive care, beta‑blockers.

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d. Subclinical hyperthyroidism pattern

Laboratory profile:

· TSH ↓ (0.01–0.4 mIU/L)

· FT4 normal

· FT3 normal

· TRAb negative unless early Graves’

Differential diagnosis:

· Endogenous: Small toxic nodule, mild Graves’ disease, resolving thyroiditis.

· Exogenous: Over‑treatment with levothyroxine (suppressive therapy for thyroid cancer).

· Physiological: First trimester pregnancy (hCG effect).

· Ageing: Very low TSH in elderly (0.1–0.4) without thyroid disease (suppressed pituitary reserve).

Outlier scenarios:

· TSH persistently <0.1, FT4/FT3 normal: Grade 2 subclinical hyperthyroidism; associated with atrial fibrillation, osteoporosis, especially age >65. Consider treatment (RAI, antithyroid drugs, or dose reduction of levothyroxine).

· TSH 0.1–0.4, asymptomatic, no nodules, negative antibodies: Grade 1 subclinical; repeat in 3–6 months. Treatment rarely needed.

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e. Central hypothyroidism pattern (secondary/tertiary)

Laboratory profile:

· TSH low, normal, or mildly elevated (biologically inactive)

· FT4 ↓

· FT3 often low

· Discordant: low FT4 with inappropriately normal/low TSH – key clue.

Differential diagnosis:

· Pituitary disease: Macroadenoma, craniopharyngioma, Sheehan syndrome, lymphocytic hypophysitis, apoplexy, irradiation.

· Hypothalamic disease: Tumour, infiltrative, traumatic, inflammatory.

· Isolated TSH deficiency: Rare; mutations in TSH‑β, TRHR, IGSF1.

· Drug‑induced: Dopamine, glucocorticoids (reversible).

· Euthyroid sick syndrome (recovery phase): May transiently mimic central hypothyroidism.

Outlier scenarios:

· Low FT4, normal TSH, no pituitary symptoms, no drugs, no illness: Consider mild central hypothyroidism; evaluate other pituitary axes, MRI pituitary.

· Low FT4, TSH 5–10 with normal bioactivity: Rare cases of biologically inactive TSH (mutations); check sex hormone‑binding globulin (low in central hypothyroidism).

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f. Euthyroid sick syndrome (non‑thyroidal illness syndrome)

Laboratory profile:

· FT3 ↓ (low T3 syndrome)

· Reverse T3 ↑ (not routinely measured)

· TSH normal or mildly suppressed (0.05–0.5 mIU/L)

· FT4 normal or low (severe illness)

Differential diagnosis:

· Any acute or chronic systemic illness (sepsis, MI, heart failure, starvation, trauma, surgery).

· Do not treat with thyroid hormone – correct underlying illness; TSH and T3 normalise spontaneously.

Outlier scenarios:

· Very low T4 + low TSH in critical illness: High mortality; thyroid hormone replacement does not improve outcome.

· Recovery phase: TSH may rise transiently (up to 20 mIU/L) with normal FT4; must not be mistaken for primary hypothyroidism.

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g. Isolated abnormal thyroid antibodies (euthyroid)

Laboratory profile:

· TSH, FT4, FT3 normal

· TPOAb and/or TgAb positive

· No symptoms

Significance:

· Marker of future hypothyroidism risk: 2–5% annual progression; more likely if TSH >2.5, young, female, high antibody titre.

· Not a disease state: No treatment indicated unless TSH rises or pregnancy planned.

· Associated with other autoimmune diseases: Type 1 diabetes, pernicious anaemia, Addison’s, coeliac disease.

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5. Best way to address aberrant levels: A holistic approach

Critical principle: Thyroid function tests are a measure of axis integrity, not a diagnosis. Do not treat an abnormal TSH without confirming the pattern, excluding interference, and establishing aetiology. Empiric levothyroxine for a “borderline” TSH without FT4 may suppress subclinical hyperthyroidism or worsen central hypothyroidism.

a. Diagnostic algorithm, not therapeutic trial

Step 1: Confirm the abnormality

· Repeat TSH + FT4 if initial abnormality is mild, isolated, or discordant with clinical picture.

· Check for biotin use – instruct patient to discontinue ≥48 hours (preferably 1 week).

· Exclude acute illness – postpone testing if patient hospitalised or acutely unwell.

· For elevated TSH with normal FT4: consider macro‑TSH (heterophile antibodies) – refer to laboratory for blocking studies or PEG precipitation.

Step 2: Identify the dominant pattern

· Primary hypothyroidism (↑TSH, ↓FT4)

· Subclinical hypothyroidism (↑TSH, normal FT4)

· Primary hyperthyroidism (↓TSH, ↑FT4/FT3)

· Subclinical hyperthyroidism (↓TSH, normal FT4)

· Central hypothyroidism (↓/N TSH, ↓FT4)

· Euthyroid sick syndrome (↓T3, N/↓TSH, N FT4)

· Isolated antibody positivity (normal TSH, normal FT4)

Step 3: Determine aetiology

· Hypothyroid patterns:

· TPOAb, TgAb (autoimmune).

· History of neck surgery, radiation, drugs (lithium, amiodarone).

· Iodine status (if clinically suspected).

· Hyperthyroid patterns:

· TRAb (Graves’ disease).

· Thyroid scintigraphy (RAIU + scan) – diffuse uptake (Graves’), patchy/nodular (TMNG/TA), low uptake (thyroiditis, factitious, iodine).

· Ultrasound (nodules, goitre, vascularity).

· Central hypothyroidism:

· Pituitary MRI.

· Other pituitary axes (cortisol, gonadal, prolactin, IGF‑1).

· Euthyroid sick syndrome:

· Diagnosis of exclusion in hospitalised patients; do not check TFT during acute illness unless strong suspicion of pre‑existing thyroid dysfunction.

Step 4: Treat the underlying cause

Primary hypothyroidism:

· Levothyroxine (LT4) – standard of care. Start dose:

· Young, healthy: full replacement 1.6 mcg/kg (≈100–125 mcg daily).

· Elderly, cardiac disease, ischaemic heart disease: start low (12.5–25 mcg), titrate slowly.

· Autoimmune hypothyroidism: LT4 lifelong.

· Postpartum thyroiditis (hypothyroid phase): LT4 for 6–12 months, then attempt withdrawal.

· Drug‑induced (lithium, amiodarone): Reduce dose or discontinue if possible; LT4 if persistent.

Subclinical hypothyroidism:

· Treat if:

· TSH >10 mIU/L (any age).

· TSH 4.5–10 with TPOAb positive, young, symptomatic, pregnant or planning pregnancy, dyslipidaemia.

· Children, adolescents.

· Observe if:

· Elderly (>70), TSH <10, TPOAb negative, asymptomatic.

Primary hyperthyroidism:

· Graves’ disease:

· Thionamides (methimazole first‑line; propylthiouracil only in first trimester or thyroid storm).

· Radioiodine (if contraindication or failed medical therapy).

· Thyroidectomy (large goitre, compressive symptoms, coexisting malignancy).

· Toxic nodular goitre / adenoma:

· Radioiodine or surgery; thionamides pre‑treatment if severely thyrotoxic.

· Thyroiditis (destructive):

· Supportive care, beta‑blockers (propranolol), NSAIDs (subacute). No thionamides or radioiodine – condition self‑limited.

Subclinical hyperthyroidism:

· Treat if:

· TSH persistently <0.1 mIU/L (grade 2) – especially age ≥65, osteoporotic, cardiac disease.

· Symptomatic, nodular disease.

· Observe if:

· TSH 0.1–0.4 (grade 1), age <65, no comorbidities, no progression.

Central hypothyroidism:

· LT4 replacement. Do not use TSH to guide dosing – follow FT4 (mid‑upper normal range).

· Check for adrenal insufficiency before starting LT4 – may precipitate adrenal crisis.

Euthyroid sick syndrome:

· No thyroid hormone therapy. Treat underlying illness.

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b. Role of supplements and holistic medicine – supportive only

Iodine:

· Iodine deficiency: Rare in iodine‑sufficient regions; if confirmed, low‑dose iodine (150 mcg/day) via iodised salt or kelp (cautious). Do not exceed – excess worsens autoimmune thyroiditis and induces hyperthyroidism.

· Autoimmune thyroiditis: Iodine supplementation not recommended; may exacerbate hypothyroidism.

· Pregnancy: Prenatal vitamins with 150 mcg iodine essential.

Selenium:

· Autoimmune thyroiditis (euthyroid or subclinically hypothyroid): 200 mcg/day selenomethionine reduces TPOAb titres and may improve thyroid ultrasound echogenicity. Does not consistently prevent progression to overt hypothyroidism.

· Mild Graves’ orbitopathy: European guidelines recommend selenium 200 mcg/day for 6 months; slows progression.

· Source: Brazil nuts (1–2 nuts/day sufficient), selenium‑enriched yeast, algae.

· Caution: Chronic toxicity >400 mcg/day (selenosis).

Zinc, copper, iron:

· Iron deficiency: Impairs thyroid hormone synthesis; correct if deficient. Avoid concurrent ingestion with LT4 (forms insoluble complexes). Separate by ≥4 hours.

· Zinc: Deficiency impairs T3 production; correct if deficient.

· Copper: Rare; excessive zinc may induce copper deficiency.

Vitamin D3:

· Deficiency common in autoimmune thyroid disease; supplement to maintain optimal levels (lichen‑derived cholecalciferol).

L‑carnitine:

· May ameliorate symptoms of hyperthyroidism (antagonises thyroid hormone entry into nucleus); weak evidence. Not first‑line.

Myo‑inositol + selenium:

· Small studies in autoimmune thyroiditis suggest improvement in TSH and TPOAb; further research needed.

Herbs and Phytochemicals from Indian subcontinent (adjunctive, not primary):

· Guggul (Commiphora mukul): Traditionally used for hypothyroidism; modern trials show minimal, inconsistent effect; may interfere with LT4 absorption. Not recommended.

· Ashwagandha (Withania somnifera): Small trials suggest modest TSH increase in subclinical hypothyroidism; long‑term safety unclear. Not for hyperthyroidism.

· Bacopa monnieri, Shilajit: Insufficient evidence; avoid concurrent use with thyroid medication.

· Never use as substitute for levothyroxine or thionamides.

· Avoid all products containing undisclosed thyroid hormone (adulterated “herbal” thyroid support).

Critical warnings:

· Do not use iodine supplements in autoimmune thyroid disease or nodular goitre – risk of exacerbation.

· Do not take calcium, iron, magnesium, or aluminium‑containing antacids within 4 hours of levothyroxine – chelation reduces absorption.

· Biotin must be discontinued before testing – may cause false hyperthyroid pattern.

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c. Dietary and lifestyle approach (plant‑forward, ecologically sustainable)

Core principles for all thyroid disorders:

· Adequate iodine intake: Iodised salt (1/2 tsp daily ≈150 mcg); seaweed (kelp, kombu) variable and potentially excessive. Avoid high‑dose kelp supplements. Plant‑based diets may be low in iodine; ensure reliable source (iodised salt, prenatal vitamins during pregnancy).

· Selenium adequacy: 1–2 Brazil nuts daily or selenium‑fortified foods.

· Avoid goitrogens in excess if iodine deficient: Cruciferous vegetables (broccoli, cabbage, kale, cauliflower), millet, cassava, soy. Cooking inactivates most goitrogens. In iodine‑sufficient individuals, no restriction necessary.

· Soy and thyroid function: Soy isoflavones do not cause hypothyroidism in iodine‑sufficient individuals; may slightly increase LT4 requirement. If consuming soy regularly, check TSH 6–8 weeks after consistent intake.

· Gluten‑free diet: Only recommended if coeliac disease or non‑coeliac gluten sensitivity confirmed; not proven to improve autoimmune thyroiditis in absence of gluten intolerance.

· Weight management: Hypothyroidism reduces metabolic rate; avoid rapid weight loss which may release stored toxins. Gradual, sustainable weight loss through plant‑forward diet and physical activity.

· Regular exercise: Improves energy, mood, cardiovascular health; safe in treated thyroid disease.

Plant‑based protein sources (ecologically responsible):

· Legumes, tofu, tempeh, edamame, quinoa, hemp seeds, spirulina, chlorella.

· No requirement for animal protein in thyroid disease management.

· Soy is safe; ensure consistent intake if on LT4 (same time, separated by ≥4 hours).

Specific considerations:

· Autoimmune thyroiditis: Consider selenium 200 mcg/day; avoid excess iodine; ensure vitamin D replete.

· Graves’ disease / hyperthyroidism: Caloric deficit may be required during weight loss after treatment; avoid stimulants (including caffeine) which exacerbate tachycardia, anxiety.

· Post‑thyroidectomy (cancer): Lifelong LT4; dietary calcium if hypoparathyroidism; no iodine restriction unless for radioiodine scanning (low‑iodine diet).

· Pregnancy: Iodine supplementation essential (150 mcg/day); LT4 dose often increases; monitor TSH every 4–6 weeks.

Note on substances with addiction potential:

This guide does not recommend tea, coffee, alcohol, or tobacco in any form. Caffeine and other stimulants exacerbate anxiety, palpitations, and insomnia in hyperthyroidism and contribute to bone loss. Alcohol directly interferes with thyroid hormone metabolism, exacerbates hepatotoxicity of antithyroid drugs, and has addiction potential. No addictive substance is necessary for the management of thyroid disease. Safe, non‑addictive lifestyle measures – particularly a whole‑food, plant‑based diet, regular exercise, and stress reduction – are both safer and more foundational for long‑term thyroid health.

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6. How soon can one expect improvement and the ideal time frame to retest

Hypothyroidism (levothyroxine therapy):

· TSH half‑life: 7–10 days for steady‑state after dose adjustment. Retest TSH 6–8 weeks after initiation or dose change.

· Once stable: Retest annually; more frequently if pregnant, malabsorption, interacting drugs, or unstable.

Hyperthyroidism (thionamide therapy):

· FT4/FT3 normalisation: 4–8 weeks after starting methimazole.

· TSH recovery: Delayed (2–4 months) – remains suppressed even after FT4 normalises.

· Retest: 4–6 weeks after initiation, then every 3–6 months during titration. After stable euthyroidism, every 6–12 months.

Subclinical hypothyroidism (observation):

· Repeat TSH, FT4 in 3–6 months, then annually if stable.

Subclinical hyperthyroidism (observation):

· Repeat TSH, FT4 in 3–6 months; if persistent grade 2 (TSH <0.1), consider treatment.

Postpartum thyroiditis:

· Hyperthyroid phase: TSH suppressed, FT4/FT3 elevated; repeat in 4–6 weeks.

· Hypothyroid phase: TSH elevated, FT4 low; LT4 if symptomatic or planning pregnancy; recheck 6–12 weeks. Attempt withdrawal after 6–12 months.

Central hypothyroidism (LT4 therapy):

· Retest FT4 (not TSH) 6–8 weeks after dose change; target mid‑upper normal range.

Amiodarone‑induced thyroid dysfunction:

· Baseline TFT before amiodarone, then every 3–6 months.

· After diagnosis, monitor monthly until stable.

Pregnancy:

· Known hypothyroidism: TSH every 4 weeks during first half, at least once each trimester thereafter.

· Newly diagnosed: immediate LT4; retest in 4 weeks.

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Conclusion

The thyroid function test panel is the most elegant bioassay of endocrine feedback in clinical medicine. Through a simple hierarchical cascade—TSH first, free T4 second, free T3 and antibodies third—it reveals not only the functional status of the thyroid gland but also the integrity of the pituitary and the presence of autoimmunity.

Do not treat an abnormal TSH in isolation. An elevated TSH with normal free T4 is not the same disease as an elevated TSH with low free T4. A suppressed TSH with normal free T4 is not the same as suppressed TSH with high free T4. Each pattern—primary, central, subclinical, destructive, euthyroid sick—carries a distinct aetiology, prognosis, and therapeutic imperative.

The holistic management of an abnormal TFT panel is therefore diagnostic precision first, cause‑specific therapy second, and supportive, ecologically sustainable lifestyle interventions third. Levothyroxine and thionamides are life‑saving, evidence‑based therapies that must never be replaced by unregulated supplements. Selenium, vitamin D, and appropriate iodine intake are adjuncts—not substitutes—for definitive treatment.

No addictive substance—whether caffeine, alcohol, or nicotine—is required for the optimisation of thyroid function. Safe, non‑addictive, ecologically responsible dietary and lifestyle interventions are always preferred.

As with all blood tests, the TFT panel is a conversation between the hypothalamus, the pituitary, the thyroid, and the clinician. Listen to the feedback loop. Investigate the discordance. Treat the patient—not the number.

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Note on dietary recommendations on this site:

For the sake of our environment we adhere to the following dietary preference hierarchy:

1. Plant‑based

2. Fungi / algae / fermented

3. Biotechnology / lab‑grown / cultures

4. Dairy / eggs

5. Meat / fish / poultry (only if no effective alternative exists)

This approach reflects ecological responsibility, antibiotic stewardship, and the urgent need to reduce the environmental footprint of dietary recommendations.

Special note on protein in thyroid disease:

Plant‑based protein sources are nutritionally adequate for all individuals with thyroid disorders, including those requiring increased protein during recovery from hyperthyroidism or post‑thyroidectomy. Soy, legumes, mycoprotein, and algae provide complete or complementary amino acid profiles. Concerns about soy interfering with thyroid function are largely unfounded in iodine‑sufficient individuals; consistent intake requires consistent levothyroxine timing. Meat and fish are neither necessary nor preferred.

Special note on addictive substances:

This guide does not recommend tea, coffee, alcohol, or tobacco in any form. Caffeine exacerbates the adrenergic symptoms of hyperthyroidism and may interfere with sleep and anxiety management. Alcohol directly suppresses thyroid function, contributes to hepatotoxicity in patients taking antithyroid drugs, and carries addiction potential. Tobacco smoke contains thiocyanates that inhibit iodine uptake and increase the risk of Graves’ orbitopathy. Safe, non‑addictive lifestyle interventions are always preferred.

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