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Diagnostics

Thyroid Testing — A Complete Panel Including Conversion and Antibodies

Most people arrive having had their thyroid tested exactly once, with exactly one marker. TSH is a good screening test and a poor description of a thyroid. It measures the pituitary’s instruction to the gland, not how much active hormone reaches the tissues that have to use it, and not whether the immune system is quietly dismantling the gland while the number still reads normal. This panel measures the rest.

Contents

What is measured · What the extra markers add · When I order it · How I read these results · What to expect · Key takeaways · FAQ · References

What is measured

A finger-prick sample, thirteen markers, processed by Eurofins Clinical Diagnostics UK. The panel is built in three parts: the thyroid axis itself, the autoimmune limb, and the downstream markers that show what the thyroid has been doing to metabolism.

The thyroid axis

Marker What it is Why it is on the panel
TSH The pituitary’s instruction to the gland The screening marker, and the one most diagnostic thresholds are written against2
Free T4 The unbound fraction of the main hormone the gland releases Largely a reservoir; it has to be converted before it acts
Total T4 (thyroxine) Bound and unbound thyroxine together Read against free T4. A discrepancy between the two points at binding-protein status rather than at the gland
Free T3 The active hormone What tissues actually use.3 Routinely omitted from NHS screening2

The autoimmune limb

Marker What it is Why it is on the panel
TPO antibodies Antibodies to thyroid peroxidase The commonest marker of autoimmune thyroid disease, often positive years before TSH moves4
Thyroglobulin antibodies (TgAb) Antibodies to thyroglobulin Adds sensitivity where TPO is negative but the picture suggests autoimmunity

What the thyroid has been doing downstream

Marker What it is Why it is on the panel
Total cholesterol Total circulating cholesterol Thyroid hormone sets the rate at which the liver clears LDL; an untreated underactive thyroid raises it7
LDL cholesterol (calculated) The fraction cleared by the hepatic LDL receptor Of the lipid markers, the one most directly tied to thyroid status7
HDL cholesterol The fraction associated with reverse cholesterol transport Read as part of the lipid pattern rather than as a target in itself
Non-HDL cholesterol Total cholesterol minus HDL A single figure for the whole atherogenic fraction
HDL:LDL ratio The two fractions expressed against each other A pattern marker, more informative than either number alone when thyroid status is changing
Triglycerides Circulating triacylglycerol Moves with insulin regulation as much as with thyroid status, which is why the two are read together
Vitamin D (25-OH) The storage form, and the standard measure of vitamin D status Deficiency is common at this latitude, correctable, and worth knowing in anyone with a positive antibody result

What the extra markers add

Three things, and each of them changes what I do rather than merely adding detail.

Free T3 tells you whether the active hormone is actually there. T4 is a precursor. It has to be converted, by deiodinase enzymes, into T3 before any cell can use it, and the same T4 can instead be routed to an inactive isomer that occupies the position without doing the work.3 Someone can therefore have a TSH and a free T4 comfortably inside the range while running short of the only form that matters at the tissue. TSH will not show you this, because TSH is responding to the T4 the pituitary sees, and the pituitary has its own local conversion. Conversion is not a fixed property of a person either: it shifts towards the inactive route in illness, in inflammation, and in sustained energy restriction — a documented adaptation rather than a fault, and one whose causes can be assessed and, where they are modifiable, addressed. Free T3 is read against symptoms, examination and the rest of the panel rather than against a threshold, because its reference range is not established as firmly as the one for TSH. [Clinical Heuristic]

The lipid markers tell you what the thyroid has been doing to metabolism. Thyroid hormone sets the rate at which the liver clears LDL from the circulation, largely by regulating how many LDL receptors the hepatocyte expresses. When thyroid function falls, clearance slows and total and LDL cholesterol rise — which is why an unexplained rise in cholesterol is a recognised reason to check thyroid function rather than to reach straight for a lipid intervention.7 [Established — review] The reading runs in the other direction too, and this is the part usually missed: cholesterol is the substrate from which every steroid hormone is made, so a low total cholesterol is not automatically a good result in someone whose complaint is hormonal. [Clinical Heuristic] Taken on the same draw as the thyroid markers, the lipids stop being a cardiovascular score and become evidence about the metabolic conditions the endocrine system is working in.

Vitamin D is measured because it is common, correctable and relevant to the autoimmune picture. Deficiency is widespread at this latitude and is straightforward to establish and correct. Observational studies report lower vitamin D status in people with autoimmune thyroid disease,8 and small randomised trials report lower antibody titres after around six months of supplementation, though not at three;9 none shows that a lower titre changes the course of the disease. [Emerging — human RCT, small] It is on the panel because vitamin D status is worth knowing in its own right, not because repleting it is a treatment for the antibodies.

Antibodies show an autoimmune process before thyroid function changes. In iodine-replete countries such as the UK, most hypothyroidism is autoimmune,4 and antibodies frequently turn positive while thyroid function is still normal. Knowing that changes the monitoring interval, and it changes how a borderline TSH is interpreted — a TSH at the top of the range means something different in an antibody-positive person than in an antibody-negative one.

What a positive antibody result is, and is not

It identifies an autoimmune process. It is not, on its own, an indication to treat. The largest randomised trials of levothyroxine in women who were antibody-positive but had normal thyroid function — TABLET and T4LIFE — did not show improved live-birth rates.5 I report that finding rather than omitting it, because it is the direct answer to the question most people ask next.

When I order it

Not from a list, and not before a history. In practice this panel earns its place when:

  • Fatigue, cold intolerance, hair or skin change, constipation or low mood have been investigated with a TSH alone and reported as normal.
  • Cycles are irregular, luteal phases short, or there is a history of recurrent miscarriage — the thyroid belongs in that assessment and is frequently the part that was not done fully.
  • Someone is already on levothyroxine, has a TSH inside the target range, and does not feel as they expect to.
  • A perimenopausal picture is being assessed, where the symptom overlap between thyroid disease and the transition is close to complete and the two are commonly confused.
  • Male presentations with low testosterone or low libido, where an untreated thyroid problem can produce the whole picture with an intact testicular axis.6
  • Body composition or metabolic markers are moving in a direction that diet and training do not explain.

Where the presenting question is broader than the thyroid, this panel is usually ordered alongside Steroid Hormone Testing or a metabolic panel rather than on its own — the reasoning for reading them together is on Hormone Optimisation.

How I read these results, and what happens next

Results come back to a consultation. I read the panel as one picture: whether the axis is producing and converting, whether the immune system is involved, and what the downstream markers say about the metabolic conditions the gland is operating in. What follows is a plan for the parts that are modifiable — nutritional status, inflammatory load, energy availability, sleep, training load — and a monitoring interval that fits the picture rather than a default.

Where something in the panel needs a doctor’s attention, I say so plainly and write to your GP or endocrinologist with the report. Diagnosis of thyroid disease, and every decision about starting, stopping or adjusting levothyroxine, is made against the TSH-led criteria set out by NICE and belongs with them.2

What to expect

A finger-prick home test by default — a small kit posted to you, the sample taken at home and returned to Eurofins Clinical Diagnostics UK. Where a finger-prick sample fails, or you would rather have a venous draw, I arrange one through a phlebotomy service. Either way the sample is taken fasted: the thyroid markers themselves do not require it, but this panel carries a full lipid profile and triglycerides respond to a recent meal, so fasting keeps every marker on the same footing and makes a repeat panel genuinely comparable with the first. If you take levothyroxine, take it after the sample on the morning of the test rather than before. If you take biotin in any form, list it in your intake form — it interferes with several thyroid immunoassays and needs a short washout.

Fee: £125, inclusive of VAT. That covers the laboratory work and the interpretation consultation — 45 minutes, in person in Wimbledon or online. Fees for every other panel are on the functional lab testing page.

A second configuration — the thyroid read against its nutritional and inflammatory inputs

The panel above carries the lipids, because for most people the metabolic terrain is what a thyroid result is missing. There is a second configuration — the thyroid panel with nutrient and inflammation markers — for the person who arrives with recent lipids already done, or whose question is what the thyroid has to work with rather than what it has been doing to cholesterol clearance.

It keeps the whole axis and both antibodies — TSH, free T4, free T3, TPO and thyroglobulin antibodies — and in place of the lipid panel it measures the inputs thyroid function depends on: ferritin (iron is required for thyroid peroxidase, the enzyme that builds thyroid hormone), active B12 and vitamin D as nutritional status, and hs-CRP as a marker of the inflammation that pushes T4 towards the inactive isomer rather than to T3. [Established — review] It is a finger-prick home test, nine markers, results in three working days.

I order it in place of the complete panel, not alongside it — when the lipids are already known, or when the nutritional question is the one that matters. It is read the same way: against history and examination, in a consultation.

Fee: £165, inclusive of VAT and the interpretation consultation.

Key takeaways

  • TSH measures the instruction to the gland. It does not measure how much active hormone reaches your tissues.
  • Free T3 shows whether the active hormone is present; total and free T4 read together show whether binding-protein status is distorting the picture.
  • Conversion shifts with illness, inflammation and sustained energy restriction — assessable conditions, not fixed traits.
  • Most hypothyroidism in the UK is autoimmune, and antibodies often turn positive before TSH moves.
  • Antibodies are informative for understanding and monitoring. Levothyroxine in antibody-positive women with normal thyroid function did not improve live births in TABLET or T4LIFE.
  • The lipids are on the panel as thyroid evidence: slowed LDL clearance points upstream, and a low cholesterol is not automatically a good result when cholesterol is the substrate for every steroid hormone.
  • Results are read in a consultation, against history and examination, rather than issued as a report.
  • One finger-prick sample, thirteen markers, with the interpretation consultation included in the fee.

Frequently Asked Questions

Why do some people not feel well on thyroid replacement even when their TSH is normal?

Because conversion of T4 to active T3 varies between individuals, and a normalised TSH does not confirm that tissue-level T3 is adequate. This is a live and unsettled question in endocrinology — combination T4/T3 therapy is permitted by European guidance as a supervised trial in selected patients, but has not on average outperformed T4 alone in randomised trials.1 What it does justify is a look at conversion, and at what conversion depends on.

My GP says my thyroid is fine. Why would I pay for this?

Frequently your GP is right, and if the full panel confirms it that is a useful thing to have established. The panel earns its place when a TSH-only result and the symptom picture disagree, when antibodies have never been checked, or when you are on treatment and still unwell. If your history does not suggest any of those, I will tell you the test is unlikely to change anything and not order it.

Can I have this done without a consultation?

No. Testing is selected after an evaluation, because the value of a wide panel is in choosing the right one for a specific question. The same clinical context is what makes the interpretation of the results, and the recommendations that follow, reliable — the free T3 and the lipid results above all, since they mean different things in different clinical contexts. If you already have recent results and want them reviewed, that is a consultation rather than a test; please upload them to your patient portal at least 24 hours ahead.

Will you tell me to stop my levothyroxine?

No. I do not start, stop or adjust prescriptions of any kind. If something in the results suggests your prescriber should look again, I will set out why in writing so you can take it to them.

Is this available on the NHS?

TSH and free T4 usually are. Free T3, the antibody panel and vitamin D are frequently not, or only in specific circumstances, which is the reason this panel exists privately.

Do I need to be off biotin or supplements first?

Biotin, yes — it interferes with several thyroid immunoassays and can distort results in both directions, so it needs a short washout. Most other supplements do not need stopping; list everything you take in your intake form.

Where is the clinic based?

Dr Ryu Natural Medicine is in Wimbledon, South West London, about ten minutes’ walk from both Wimbledon and South Wimbledon stations; the entrance is on Southey Road. Directions and parking are on the access and parking page.

References

  1. Wiersinga WM, Duntas L, Fadeyev V, Nygaard B, Vanderpump MPJ. 2012 ETA guidelines: the use of L-T4 + L-T3 in the treatment of hypothyroidism. Eur Thyroid J. 2012;1(2):55–71. doi:10.1159/000339444 [Established — clinical guideline; area contested] ↩︎

  2. National Institute for Health and Care Excellence. Thyroid disease: assessment and management (NG145). Published 20 November 2019. Recommendations 1.2.8–1.2.9 (TSH-led testing), 1.3.3–1.3.4 (levothyroxine first line; liothyronine not routinely offered) and 1.5.2–1.5.3 (subclinical hypothyroidism). https://www.nice.org.uk/guidance/ng145 [Established — clinical guideline] ↩︎↩︎↩︎

  3. Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev. 2002;23(1):38–89. doi:10.1210/edrv.23.1.0455 [Established — review] ↩︎↩︎

  4. Vanderpump MPJ. The epidemiology of thyroid disease. Br Med Bull. 2011;99:39–51. doi:10.1093/bmb/ldr030 [Established — review] ↩︎↩︎

  5. Dhillon-Smith RK, Middleton LJ, Sunner KK, et al. Levothyroxine in women with thyroid peroxidase antibodies before conception. N Engl J Med. 2019;380(14):1316–1325. doi:10.1056/NEJMoa1812537 [Established — human RCT, null] · van Dijk MM, Vissenberg R, Fliers E, et al. Levothyroxine in euthyroid thyroid peroxidase antibody positive women with recurrent pregnancy loss (T4LIFE trial): a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Diabetes Endocrinol. 2022;10(5):322–329. doi:10.1016/S2213-8587(22)00045-6 [Established — human RCT, null] ↩︎

  6. Krassas GE, Poppe K, Glinoer D. Thyroid function and human reproductive health. Endocr Rev. 2010;31(5):702–755. doi:10.1210/er.2009-0041 [Established — review] ↩︎

  7. Duntas LH, Brenta G. A renewed focus on the association between thyroid hormones and lipid metabolism. Front Endocrinol. 2018;9:511. doi:10.3389/fendo.2018.00511 [Established — review] ↩︎↩︎↩︎

  8. Wang J, Lv S, Chen G, et al. Meta-analysis of the association between vitamin D and autoimmune thyroid disease. Nutrients. 2015;7(4):2485–2498. doi:10.3390/nu7042485 [Established — human observational] ↩︎

  9. Wang S, Wu Y, Zuo Z, Zhao Y, Wang K. The effect of vitamin D supplementation on thyroid autoantibody levels in the treatment of autoimmune thyroiditis: a systematic review and a meta-analysis. Endocrine. 2018;59(3):499–505. doi:10.1007/s12020-018-1532-5 [Emerging — human RCT, small] ↩︎


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Dr Ryu Natural Medicine is in Wimbledon, South West London. Testing is selected after assessment, so the place to start is a consultation rather than a blood form.

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