The Claim
Type 2 deiodinase (D2) activity in the anterior pituitary is resistant to T4-induced degradation, permitting sustained T3 production despite elevated T4 levels, while D2 activity in skeletal muscle and bone marrow is rapidly inactivated by T4, resulting in cessation of T3 production.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
In the anterior pituitary, the enzyme D2 remains active even when T4 levels increase, continuing to produce T3. In skeletal muscle and bone marrow, the same enzyme is quickly turned off by T4, stopping T3 production.
See the scientific wording
Type 2 deiodinase (D2) activity in the anterior pituitary is resistant to T4-induced degradation, allowing sustained T3 production even when T4 levels rise, whereas D2 in skeletal muscle and bone marrow is rapidly inactivated by T4, leading to loss of T3 production.
In the pituitary gland, the enzyme that converts T4 to T3 stays active even when T4 levels rise, so T3 keeps being made and shuts down TSH production. In muscle and bone marrow, the same enzyme breaks down quickly when T4 rises, so T3 production stops completely.
What the research says
1 studyStudy: Sustained pituitary T3 production explains the T4-mediated TSH feedback mechanism.
In the pituitary gland, the enzyme that turns T4 into T3 keeps working even when T4 levels go up, so T3 keeps being made. But in muscle and bone marrow, that same enzyme shuts off completely when T4 rises, stopping T3 production — and the study proved this exact difference.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.