LISTEN to an audio interview with leading US endocrinologist Dr. Antonio Bianco in March 2018.
He explains why T4 monotherapy became so successful, and why the addition of T3 medication to some thyroid patients’ therapy may be helpful in removing chronic hypothyroid symptoms.
In this post we give you a commentary.
The first 3 minutes provide several audio “quotations” before the whole interview begins. These are truly the high points of the interview. The page also has some excellent infographics on it.
Keep in mind, Bianco is a mainstream endocrinologist, not someone on the fringes of his discipline. From Bianco’s bio: “He has been recognized with a number of national and international awards and membership in prestigious medical societies. A well-rounded investigator in the field of thyroid disease, Bianco led two American Thyroid Association task forces: one charged with drafting guidelines for thyroid research (as chair) and another responsible for developing guidelines for the treatment of hypothyroidism (co-chair).”
DISAPPOINTING, YET REVEALING.
As much as we respect and honor Bianco for his research and patient advocacy, listening to him gives some idea of what is holding back many doctors and medical systems from accepting T3 therapy.
Some of Bianco’s interview expresses the widespread skepticism about using Free T3 levels or symptoms as goals in therapy. He expresses the perceived drawbacks or limitations of T3 therapy compared to T4 therapy.
COMBINATION THERAPY TRIALS
Desiccated thyroid (NDT / DTE) is the original combination T4-T3 therapy that has been tested on millions of patients since the 1890s. It has a T3:T4 ratio of approximately 1:4 (20% T3, 80% T4)
Many of the modern clinical trials of T3-T4 synthetic combo therapy limit the ratio of T3:T4 to 1:14 or lower. They believe they are giving a more “physiologically correct” ratio than desiccated thyroid, but their ratio is not based on achieving physiologically optimal free T3 levels or T3:T4 ratios in blood, nor on resolving patient symptoms.
Bianco discusses his use of restrictive T3 doses such as 2.5 – 5 mcg of T3 twice a day.
These trials also often attempt to prevent TSH from dropping below range as the only criterion of optimization. They go ahead and dose what they think is best according to the patient’s pituitary gland and then they ask the patient afterwards how they feel.
Therefore, it’s no wonder that clinical trials of such restrictive T3-T4 ratios and doses show hardly more than placebo effect.
It’s as if they want this trial to fail for all but a small minority of patients whose T3 is extremely low before the trial.
DESICCATED THYROID
At 22:00 Bianco discusses NDT. He believes that patients on this medication experience heart symptoms like palpitations because the T3 content is too high. If it is so harmful, why are so many patients fine on this therapy in long term experience? No patient voluntarily stays on a medication that continues such distressing symptoms when they could so easily switch back to synthetic T4 therapy.
He acknowledges that the 2017 ATA patient survey results (12,000+ patients) show NDT got a higher satisfaction rating than T3-T4 synthetic combo therapy, and T3-T4 combo therapy got a higher rating than T4 monotherapy.
Sadly, he dismisses the survey’s methodology, saying that it’s likely that mostly grumpy patients took the survey. Shockingly, he also says that the brains of patients taking T3 are stimulated so of course they are happy, but it doesn’t mean they’re healthier. What, is it like they are taking cocaine? This is a natural hormone that our body needs, not a chemical. If it resolves our cognitive symptoms and depression that is like being on a “stimulant”?
THYROID TESTING
He also says that when HE treats a patient with T4 alone, he only measures TSH. Despite all he says about reduced T3 levels on this mode of therapy, he still trusts that when “the pituitary is happy” the right dose is achieved. Very contradictory and disappointing, but he can’t say otherwise and still be an award-winning endocrinologist who is asked to lead task forces that write thyroid therapy guidelines.
When he treats with T3-T4 combination, he measures T3. Why? Because it helps him limit T3 doses. He is afraid of spiking T3 above normal reference range levels and if he sees this happening, he cuts back T3 dose. He probably tells his patients to take their blood test 3-4 hours after their T3 dose to see how high it goes, instead of seeing how low it goes 18 hours after a dose.
SYMPTOMS
In discussing hypothyroid symptoms, he dismisses them too much:
Depression, he says, can be caused by “just being depressed.” With TSH of 3.5 he believes a doctor should not treat the patient with T4, because treatment will label / diagnose the patient as hypothyroid. He does not discuss the possibility that measuring T3 and treating with T3 could resolve the depression.
He then admits matched patients taking levo are more overweight by 10 pounds compared to matched controls, but he doesn’t blame levothyroxine therapy, he says “you have to watch your weight” and “police” yourself in your physical activity.
Being on levo will also make depression symptoms more likely, he says, but just like the case of being overweight, this news should just make you more vigilant about depression and go talk to a therapist if you feel depressed. But we can’t blame the levo therapy, no. (Dear Bianco, you hesitate to blame because you don’t collect data on their T3 levels, just their TSH)
WAITING FOR THE PERFECT T3 PHARMACEUTICAL
Finally, he sets the bar too high for T3 pharmaceutical delivery.
He says only if and when we create a system that delivers T3 at a constant rate, can we determine if T3 therapy is truly good for people.
He does not mention studying the patients who have lived for decades with T3 in their therapy, delivered without these fancy high-tech future methods.
So we have to wait for some very expensive T3 medication to come on the market because we can’t take the risk that our fluctuating T3 levels just might harm us? Meanwhile patients on full T3 therapy are doing fine for decades?
Here’s a question for you Dr. Bianco: Why do you think having fluctuations in T3 levels will harm us more than being continually low in T3 would harm us, by sapping our life away?
Where is the evidence of harm? Why are you fearful of something you don’t have evidence for? That’s not evidence-based fear. That is simply fear of the unknown. Fill the evidence gap. Get to know some happy T3-only patients and their doctors.
OUR CONCLUSIONS
As thyroid patients who have done a lot of reading in the medical literature AND have experienced and observed T3 therapy in our patient community, we see the “peaks and valleys” of T3 dosing not as drawbacks or risks or limitations, but rather simply differences between the way T4 and T3 work.
The evidence from science informs those of us who successfully resolve hypothyroidism with T3.
We see doctors’ current preference for T4 therapy as a signal of the desire to conform to what they are told by their peers is “evidence-based,” what they are familiar with and what they’ve been trained to manage with, and what is perceived as simpler for themselves to manage (with one test, the TSH, and one pill, T4).
Many doctors forget that the doctors of the past were just as reluctant to adopt synthetic T4 therapy in the 1970s because desiccated thyroid was so well known, so effective, and so simple to manage.
Great blog, I recently found – one of the biomarkers much in focus is lipids and Bianco et al have written this fine article : Systemic Thyroid Hormone Status During Levothyroxine Therapy in Hypothyroidism: A Systematic Review and Meta-Analysis – https://academic.oup.com/jcem/article-abstract/103/12/4533/5074280