Thyroid Blood Markers

Pituitary hormone that controls thyroid gland output.

PED: T3 supplementation (cytomel, common in contest prep) will suppress TSH. Prolonged suppression can take weeks to recover. Trenbolone may affect thyroid function in some individuals.

Active thyroid hormone. Controls metabolic rate.

PED: May be affected by severe caloric restriction during contest prep. T3 supplementation reduces T4 production through feedback. Important to check alongside TSH.

Most active thyroid hormone. Directly affects metabolic rate.

PED: Exogenous T3 use will show elevated Free T3 with suppressed TSH and T4. Contest prep caloric restriction naturally lowers T3 (metabolic adaptation). GH can improve T4-to-T3 conversion.

An inactive isomer of T3 produced when the body converts T4 down the alternative deiodination pathway. Reverse T3 has no thyroid-hormone activity but competes with active T3 at the cellular level. It rises when the body deliberately downregulates metabolism, so it is used as a marker of non-thyroidal illness and metabolic stress rather than of primary thyroid disease.

PED: Directly relevant to hard-dieting and contest-prep athletes. Aggressive caloric restriction, very low body fat, overtraining, illness, and high cortisol all shift T4 conversion away from active T3 and toward reverse T3, the classic euthyroid sick syndrome (low T3 syndrome) picture: normal or low-normal TSH, low Free T3, and a raised rT3. This is an adaptive slowdown, not primary hypothyroidism, and it typically reverses with refeeding and recovery rather than with thyroid medication. Exogenous T4 can raise rT3 (more substrate for the inactive pathway), whereas exogenous T3 (Cytomel) bypasses conversion and tends to lower endogenous rT3. A high rT3 with low Free T3 in a lean, heavily-dieting athlete signals metabolic adaptation and the need to restore energy availability. The Free T3 to reverse T3 ratio is sometimes used to gauge tissue-level thyroid status.

Autoantibodies against thyroid peroxidase. Elevated levels are the hallmark of Hashimoto's thyroiditis (autoimmune hypothyroidism).

PED: AAS reduce thyroxine-binding globulin (TBG), causing total T3/T4 to appear low while free hormones remain unchanged — this is not autoimmune. GH increases T4-to-T3 conversion and can unmask latent thyroid insufficiency if anti-TPO is borderline. Exogenous T3 (Cytomel) suppresses TSH, which can mask rising anti-TPO. If symptoms like fatigue, weight gain, or poor recovery persist post-cycle, check anti-TPO alongside TSH and Free T4 to rule out Hashimoto's.

Autoantibodies against thyroglobulin, a protein produced by the thyroid gland. Elevated levels indicate autoimmune thyroid disease, most commonly Hashimoto's thyroiditis. Also used in thyroid cancer monitoring, where TgAb interferes with thyroglobulin tumour marker assays.

PED: AAS are broadly immunosuppressive and may suppress autoantibody production, so TgAb may appear deceptively low on-cycle. Check during off-cycle or cruise periods for a more accurate reading. GH increases T4-to-T3 conversion and may unmask latent autoimmune thyroiditis in susceptible individuals. Exogenous T3 (Cytomel) profoundly suppresses TSH, which can mask a developing autoimmune process. After T3 discontinuation, TSH rebound can amplify the autoimmune response and temporarily spike TgAb.

An antibody that binds the TSH receptor and switches it on, driving the thyroid to overproduce hormone independently of TSH. The specific cause of Graves' disease.

PED: This is the test that names the cause when thyroid function is genuinely overactive. That matters here because the picture it produces can be mistaken for something self-inflicted: suppressed TSH with raised free T4 and free T3 looks superficially like exogenous thyroid hormone use, and someone running T3 or T4 who develops Graves' can have it written off as their own dosing. The distinction is straightforward on paper. Exogenous T3 suppresses TSH while thyroglobulin falls and antibodies are absent; Graves' suppresses TSH with positive TSI and usually a diffusely enlarged gland. Do not interpret this while running thyroid medication without telling the clinician, because the two states are easy to confuse and the treatments are opposite. Also note that raised TSI in pregnancy crosses the placenta and can affect the fetal thyroid, so it carries weight beyond the person tested.

The total amount of thyroxine (T4) in serum, including both the small free (active) fraction and the large fraction bound to carrier proteins such as thyroxine-binding globulin (TBG), transthyretin, and albumin. Because it measures bound plus free hormone, Total T4 moves whenever binding-protein levels change, unlike Free T4 which reflects only the unbound hormone.

PED: Total T4 is heavily influenced by binding proteins, so it can shift without any true change in thyroid status. Oral oestrogens (and the altered hepatic protein synthesis seen with some AAS use) raise TBG and push Total T4 up, while high-dose androgens can lower TBG and Total T4, in both cases with normal Free T4 and normal thyroid function. Pregnancy raises it too. For monitoring thyroid status on cycle, TSH plus Free T4 (or Free T3) are more reliable than Total T4. Total T4 is mainly useful as part of the legacy Total T4 x T3 Uptake calculation (the Free T4 Index) when a direct Free T4 is unavailable.

An indirect, legacy measure of how saturated the thyroid-binding proteins are with hormone, also reported as the Thyroid Hormone Binding Ratio (THBR). It does NOT measure T3 levels directly; it moves inversely to the number of unoccupied binding sites on thyroxine-binding globulin. It is used together with Total T4 to calculate the Free T4 Index and correct for binding-protein variation.

PED: T3 Uptake is a binding-protein test, not a thyroid-activity test. When TBG rises (oral oestrogen, pregnancy, some AAS-related hepatic effects) there are more free binding sites, so T3 Uptake falls; when TBG falls (high-dose androgens, nephrotic states) T3 Uptake rises. Read alongside Total T4: a high Total T4 with a low T3 Uptake suggests raised binding proteins rather than hyperthyroidism, whereas both moving in the same direction suggests a true thyroid change. Most modern panels replace this with a direct Free T4, so treat it mainly as an input to the Free T4 Index.

A calculated estimate of free thyroid hormone, historically called T7, derived by multiplying Total T4 by the T3 Uptake fraction. By combining a total hormone level with a binding-protein measure, it corrects for changes in binding proteins and approximates what a direct Free T4 assay measures. It is a legacy calculation from the era before reliable direct Free T4 tests.

PED: The Free T4 Index exists to strip out binding-protein noise: if Total T4 is high only because oestrogen or AAS-related changes raised TBG, the accompanying low T3 Uptake pulls the index back into the normal range, correctly indicating normal thyroid status. This makes it more informative than Total T4 alone in athletes whose binding proteins are shifted by oral oestrogens or high-dose androgens. That said, the modern direct Free T4 assay already in this knowledge base is the preferred test; the index is mainly seen on older or budget panels. Reference ranges are strongly method-dependent, so compare against the reporting lab's own range.