Treating T3 Deficiency, The Evidence you Need - Part 6

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Course Description

Dr. Rouzier covers the poor research articles that confuse many physicians into not prescribing thyroid.  In order to understand the opposition, you need to understand the flawed research and thinking from the experts.  Dr. Rouzier explains how Graves Disease has impacted the study findings and the harm that occurs when subclinical hypothyroidism goes untreated.

Objectives:

Upon completion of this workshop, the healthcare professional will be able to:

1. Review 3 recent studies demonstrating that T4 thyroxine does not improve symptoms of hypothyroidism and therefore should not be used to treat subclinical hypothyroidism.
2. Review other association papers and opinions that elevated levels of thyroid hormone and concomitant TSH suppression are associated with significant harm, sudden cardiac death, and osteoporosis remember ADNPC.
3. Recall that the authors of the foregoing studies do not understand that ADNPC and the harm of Graves’ disease should not be extrapolated to exogenous thyroid replacement.
4. Discuss where the addition of T3 improves symptomatic patients whereas the use of thyroxine does not.
5. Review the data demonstrating that T4 thyroxine can suppress T3 levels which in turn can make hypothyroid symptoms worse, not better.
6. Review the literature whereby TSH suppression is not synonymous with clinical hyperthyroidism.
7. In reviewing any study, it is important to ascertain if the conclusions to the study reflect an evaluation of baseline lab values versus evaluation of treatment levels and the resultant outcomes.  Again, baseline observation studies should not be extrapolated to what happens when one gives the hormone, particularly with regard to thyroid hormone.
8. Discuss the meta-analysis demonstrating that endogenous Graves’s hyperthyroidism is associated with a 20% increased risk of sudden cardiac death, a-fib, stroke, PE and cancer.
9. Recognize that these risks occur in patients after treatment for Graves’ disease that have an autoimmune disease that causes the morbidity, not thyroid hormones.  Even after the thyroid gland is ablated and normal levels of thyroid hormone are restored.  The disease continues to progress despite “normal” thyroid levels.