Source comparison
BPC-157 Research Thyroid Considerations: Comparison
TSH 0.4–4.5 mIU/L (functional optimal: 2.5 mIU/L) indicates the pituitary is compensating for reduced thyroid output, which limits metabolic capacity un
This comparison does not assign a generated winner or score.
- TSH
- 0.4–4.5 mIU/L (functional optimal: <2.5 mIU/L)
- Pituitary signalling to thyroid gland. Reflects thyroid gland output sufficiency
- Elevated TSH (>2.5 mIU/L) indicates the pituitary is compensating for reduced thyroid output, which limits metabolic capacity under increased demand
- Essential baseline. But insufficient on its own to rule out thyroid insufficiency
- Free T4
- 0.8–1.8 ng/dL
- Thyroid hormone storage form. Converted to active T3 in peripheral tissues
- Low-normal free T4 (<1.0 ng/dL) suggests limited thyroid hormone reserve, which can bottleneck T3 production during high metabolic demand
- Pair with free T3. T4 in mid-range with low T3 reveals conversion issues
- Free T3
- 2.3–4.2 pg/mL
- Active thyroid hormone driving mitochondrial ATP production and protein synthesis
- Low-normal free T3 (<2.8 pg/mL) is the single most predictive marker for impaired recovery during peptide protocols. Tissue repair requires sustained T3 signalling
- Most critical marker. BPC-157 efficacy depends on adequate intracellular T3
- Reverse T3
- <20 ng/dL
- Inactive metabolite produced under stress. Blocks T3 receptor binding
- Elevated rT3 (>20 ng/dL) indicates thyroid hormone resistance at the cellular level, rendering normal T3 levels functionally insufficient
- Elevated rT3 explains 'non-response' to peptides despite normal TSH and T4
- TPOAb
- <35 IU/mL
- Antibodies attacking thyroid peroxidase. Marker of autoimmune thyroid disease (Hashimoto's)
- Positive TPOAb indicates progressive thyroid destruction, increasing risk of decompensation under metabolic stress from peptide protocols
- Identifies researchers at high risk for thyroid dysfunction during extended protocols