High Dose Replacement and Thyroid Optimization
The previous course on thyroid optimization was intended to contrast and explain how and why the endocrine societies and the ATA frighten us into not using thyroid hormone. I introduced the concepts that the endocrinologists use when treating hypothyroid patients as well as their reluctance to prescribe thyroid hormone to SC hypothyroid patients. Despite the plethora of data and studies proving that patients DON’T improve on T4-alone therapy, the ATA and AACE reject all the studies demonstrating that patients DO benefit when T3 is added to T4, but also when DTE is used preferentially in place of T4-alone or T4 and low dose T3. When used correctly, most recent literature overwhelming proves that patients prefer DTE over any other thyroid preparation.
A Review of the Studies on TSH Suppression
The last medical journal article that was presented in the last course, Treating T3 Deficiency: The Evidence You Need (Part 6), stated that exogenous hyperthyroidism (TSH suppression) with thyroid hormone administration was not associated (causative) of any adverse effect. “There is no scientific evidence that the clinical impact of TSH suppression is significant.” This meta-analysis proving no harm with thyroid hormone administration (along with TSH suppression) is in direct contrast to the opinions of the other papers/authors opinions reviewed in the last course. I reviewed many papers and opinions that TSH suppression was harmful. However, I emphasized that the studies cited were all studies that reviewed baseline TSH levels in patients with Graves’ disease. Not one study was an outcome study in patients that were prescribed/treated with thyroid hormone. However, the results of all these baseline observation studies demonstrated/proved that suppressed TSH levels (in Graves’ patients) were associated with harm, sudden cardiac death, a-fib, osteoporosis, etc. The authors of the various opinion papers went on to extrapolate that thyroid hormone administration resulting in suppressed TSH levels (biochemical hyperthyroidism) was just as bad/harmful as that seen in those studies citied in patients with Graves’ disease. Nothing could be further from the truth. That which is observed in treatment trials can be completely the opposite of what is observed in baseline observation studies. Another perfect example of ODNPC.
Recent Literature Supports That Low Free T3 was the Highest Independent Predictor of Death in CV Patients
More Proof and Reasoning that T4 Monotherapy Results in Inadequate Conversion