Treating T3 Deficiency Why T4 Thyroxine Therapy does not Improve Symptoms and Why TSH Suppression does NOT Result in Harm
Why T4 Thyroxine Therapy does not Improve Symptoms and Why TSH Suppression does NOT Result in Harm by Neal Rouzier, MD On Day 1 of the Part I BHRT Workshop
In the first course, Testosterone for Women (Part I), I reviewed the current controversy in prescribing testosterone to women. In a separate consensus paper that is different from the one discussed in the first course, the authors recommend testosterone replacement based on symptoms and signs and not on serum levels. In fact, in this second consensus paper from “experts that have experience in the field of testosterone administration,” the authors stressed the importance of replacing testosterone to improve symptoms and not by being guided by numbers or levels. These authors specifically emphasized that testosterone should be supplemented based on symptoms and not just on serum levels alone, as testosterone levels do not correlate with symptoms as per much of the medical literature. The authors also suggested that testosterone should be dosed and adjusted based on symptom improvement, and not by testosterone levels. The authors reiterated that no number (or testosterone level) denotes a deficiency as symptoms denote a deficiency. Furthermore, improvement in symptoms do not correlate with numbers either as all women will respond differently and not based on any number. So, in contrast to men where the guidelines state that we must follow levels and numbers, these guidelines for women recommend that we do not test baseline levels nor treatment levels, rather symptoms should guide treatment initiation.
A 45 year old female presents to you complaining of fatigue, loss of energy, weight gain, muscle pain, and weakness in exercising.
She read about the benefit of hormones in treating her condition, but her PMD is against the use of hormones. Although she is open to taking hormones, her PMD scared her into thinking that testosterone is somehow harmful. You assure her that testosterone is not harmful and that many of her symptoms will improve on testosterone supplementation.
Previously, we discussed how patients are taking more medications and experiencing an endless conundrum of health issues. The systemic failure to address the root causes of disease is a huge part of the problem. Along with the proven benefits of a healthy diet, exercise, and stress management, we can greatly improve health outcomes by utilizing another evidence-based strategy: bioidentical hormone replacement therapy, or BHRT.
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.
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.
Controlling HgBA1C with Medications Does not Make Diabetes Disappear – It Lowers the Surrogate Marker HgBA1C
Although the pathophysiology is simple, the treatment and reversal of CVD and cancer is what is so confusing, complex, misunderstood, and ignored.
Recent Literature Supports That Low Free T3 was the Highest Independent Predictor of Death in CV Patients
Recent Literature Supports That Low Free T3 was the Highest Independent Predictor of Death in CV Patients Written by Neal Rouzier, MD Recommended Pre-Reading: More Proof and Reasoning that T4
More Proof and Reasoning that T4 Monotherapy Results in Inadequate Conversion Written by Neal Rouzier, MD Recommended Pre-Reading: If T4 Does not Improve Symptoms, and Normalizing TSH Does not Guarantee
If T4 Does not Improve Symptoms, and Normalizing TSH Does not Guarantee or Infer Improvement in Symptoms, Then How Should we Treat Patients?
If T4 Does not Improve Symptoms, and Normalizing TSH Does not Guarantee or Infer Improvement in Symptoms, Then How Should we Treat Patients? Written by Neal Rouzier, MD Recommended Pre-Reading: