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.

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.