- Focusing on TSH alone as the primary indicator of thyroid function is inadequate. Conventional thinking is that if TSH is normal then your symptoms are not related to the thyroid (e.g. fatigue, depression, thinning hair, cold intolerance, dry skin, etc.). The biochemical classifications of ‘normal/subclinical/hypothyroid’ based on TSH are arbitrary as symptoms can exist with ‘normal’ TSH levels and vice versa. Context and clinical symptoms are key, the free T3 at the cellular level is responsible for the majority of thyroid hormone’s actions. Providers are reluctant to measure free T3 as this is not the way we were trained and the guidelines advise against it.
- LT4/synthroid has been the treatment of choice since the 1960s. A substantial number of patients on LT4 (~10-20%) will continue to endorse symptoms and poor quality of life despite normalization of TSH. Biochemical euthyroidism is ultimately hollow without symptomatic relief. The fear of using T3 in the treatment plan is related to perceived risks of atrial fibrillation and osteoporosis which are unfounded and extrapolated from Graves’ disease. Also, the paradigm that the body will make whatever T3 it needs from T4 completely discounts heterogeneity in our genetic machinery related to the chemical processes involved in the conversion of T4 to T3.
- Optimizing thyroid function and suppressing (not normalizing) TSH will lead to improved symptoms (fatigue, brain fog, depression, etc.), better metabolism, and ameliorated cardiovascular risk. Working with an experienced provider to get a full panel of thyroid testing and in the context of symptoms, then deciding on appropriate interventions which may involve nutrition and/or replacement is crucial.