A Review of the Studies on TSH Suppression

A Review of the Studies on TSH Suppression

Treating T3

A Review of the Studies on Suppressed TSH Levels

Written by Neal Rouzier, MD

Treatment Scenario

Your hormonally optimized 45 y/o female patient requests an office visit to discuss her thyroid hormone. Her PMD chastises her for taking thyroid hormone and states that he does not wish to see her anymore as a patient. She relates that upon routine testing of thyroid function, that the TSH level was too suppressed and that she could suffer a stoke or blood clot by taking too much thyroid. She is concerned because her doctor scared her. She wants you to call up the doctor and explain that the thyroid hormone she is taking is not harmful and is safe.

You politely decline the opportunity to speak with her PMD. Instead, you offer her several papers to read and schedule her back for a visit to discuss the papers. You must convince her that her doctor is doing everything correct as that is the way that we are all taught and trained. However, her doctor will not understand that the TSH suppression does not result in the same harm as Graves’ disease and that it is too complex to explain.

The patient feels well on the thyroid regimen and wishes to continue the doses as prescribed but requires reassurance as her doctor scared her. She also agrees to stop the thyroid hormone a week before seeing her PMD so as to not upset her PMD when he retests her thyroid levels at every visit (which he will continue to do at every visit forever).

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.

Haven’t taken training with us yet, but interested in learning more about the value and efficacy of BHRT as an alternative to medication-based therapies? Please consider our four part Hormone Optimization Workshop Series, and start training with us at Part I: Discover the Power of BHRT.

If you are interested in learning more about treating T3 deficiency, please consider taking our thyroid series.

Table of Contents


I find it absolutely amazing that relatively intelligent doctors still do not understand basic principles of study interpretation and in performing/designing studies. The fact that these authors’ comments and extrapolations in their opinion papers got published is also amazing, unfortunate, and downright harmful in that it misleads practitioners to assume thyroid hormone administration that results in high levels of thyroid hormone and TSH suppression is harmful. This is in fact not true. Our peers and endocrinologists will not understand/comprehend this, but you should. You should also appreciate that your patients PMDs will not understand this, and most will completely disagree with it as it was not what they, you and I were taught. As the result, this webinar is the most important webinar to understand when prescribing thyroid hormone. The concepts are complex and not understood by most physicians as they (our peers) don’t understand the basics that observation does not prove causation, or ODNPC. In order to prove harm of thyroid hormone and TSH suppression, one must study it in outcome studies (RCTs are Grade A evidence) and not baseline observation studies (in Graves’ patients) that prove nothing (Grade D studies). And don’t waste time trying to explain this as your peers will reject this as it is again different from what we were originally taught and trained (and misled to believe).

In our first paper in this course, epidemiology studies demonstrate that hyperthyroidism is associated with an increased risk of CHD, a-fib, and osteoporotic fractures. Remember this was in endogenous hyperthyroidism in patients with Graves’ disease and not in patients treated with thyroid hormone. Similarly, patients with hypothyroidism developed CVD. One must understand that the harm of Graves’ disease is due to an autoimmune disorder and not due to thyroid hormone as the harm persists long after the thyroid hormone level has been corrected. One must understand that correcting the excess thyroid hormone level did not reverse or prevent the complications of the autoimmune dysfunction of Graves’ disease. Thyroid treated patients also preferred TSH levels to <0.1 or suppressed. The study showed that this strategy was safe.

In the next study, patients that had their thyroid glands removed experienced complete loss of T3 production. When T4 was replaced, it resulted in very high T4 levels and very low T3 levels. Only markedly suppressed TSH levels from T4 administration resulted in premorbid T3 levels. Remember the authors that stated how harmful TSH suppression was? Now the studies proved that only TSH suppression to zero resulted in improvement in symptoms and normal Free T3 levels. Oh, how the pendulum swings. This is one of those papers that I frequently give to peers with the admonition, “Here, read this!” Suppressed TSH levels do not cause harm and are frequently necessary in order to provide adequate premorbid (pre-surgery) FreeT3 levels. Patients remain symptomatic of low thyroid when their Free T3 levels remain low.

Finally, there is one more study showing that subclinical hyperthyroidism (in untreated patients that were not being treated with thyroid hormone) results in increased CHD, CVD mortality, and all-cause mortality. Again, authors emphasized that these were baseline thyroid hormone levels measured in untreated patients and therefore were in patients with Graves’ disease. This observation study did not evaluate patients that were treated with thyroid hormone. All levels were done at baseline and not on any thyroid hormone, indicating that all levels that were found to be elevated were in Graves’ disease patients.

Finally, a meta-analysis demonstrated Graves’ hyperthyroidism was associated with increased mortality from CVD, cardiac arrhythmias, strokes, PE, and cancer. Patients with Graves’ disease were either treated with I-131 radiotherapy or surgery. Increased mortality remained after definitive therapy out to eight years, and this was after the hyperthyroidism was corrected, ie, the patients had normal thyroid hormone levels and normal TSH levels but still went on to experience increased mortality. Why did they still continue to experience increased mortality when their Graves’ hyperthyroidism was treated and corrected? It was not due to increased thyroid hormone as that was treated and corrected with definitive therapy with subsequent normalization of thyroid function with T4.  Obviously, it was due to the autoimmune disorder and not due to thyroid hormone which was now normal. Thus, one cannot assume or extrapolate that the harm of Graves’ disease hyperthyroidism was due to thyroid hormone (which was normalized) but rather due to the autoimmune disorder that causes the Graves’ disease that persists even after normalization of thyroid function. Unfortunately, our peers will not understand this and will continue to blame/associate/extrapolate a suppressed TSH level to result in the same harm as Graves’ disease. Or that it was due to excessive amounts of thyroid hormone. It is extremely important for us to make this distinction that a suppressed TSH level does not result in the same harm as Graves’ disease. Unfortunately, based on the prior studies reviewed in this webinar, our peers will not be able to make this distinction. Even the experts don’t grasp or comprehend this.

Haven’t taken training with us yet, but interested in learning more about the value and efficacy of BHRT as an alternative to medication-based therapies? Please consider our four part Hormone Optimization Workshop Series, and start training with us at Part I: Discover the Power of BHRT.

T3 pt 1

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