Here, I comment on a brief October 2018 article in a journal of the American Thyroid Association — the association that writes the guidelines that dismisses Free T3 testing and T3/T4 therapy.
Link: https://www.liebertpub.com/doi/full/10.1089/ct.2018%3B30.523-525
This article shows the leading endocrinologists are getting worried about doctors not adhering to guidelines.
They did a study that showed that doctors are being tempted to prescribe T3/T4 combo therapy in certain patients who have symptoms and low Free T3 levels.
They can’t stop patients from complaining of symptoms, so perhaps one way to stop this trend is to disallow them from measuring Free T3, which may actually tip the balance in helping the doctors see that the patient may need T3.
Commentary or ridicule?
The “Commentary” at the end of this article shows that the ATA is concerned about this shocking (“surprisingly striking”) trend.
They try hard to rein in their emotions but you can see that they are thrusting “evidence” in the face of these misled doctors.
How un-evidence-based it is that doctors would take such risks (gasp) to prescribe such therapies!
“Look!” they are saying, “the patient’s hypothyroidism has undergone “biochemical correction!”
Biochemical correction?
Of course, they are asserting their dogma that TSH “normalization” alone is the biochemical sign that hypothyroidism has been corrected.
They therefore dismiss the doctor’s evidence of a patient’s low Free T3.
They can’t admit the evidence that biology has proven suboptimal T3 in organs and tissues IS hypothyroidism. For example, let’s just pick one organ, the LIVER:
The levels of thyroid hormone and thyroid binding proteins are altered in patients of chronic liver disease. Low free T3 syndrome is frequently described in patients with cirrhosis of liver and is characterized by increased rT3, low T3 and decreased T3:T4 ratio
(“Thyroid Profile in Patients of Cirrhosis of Liver: A Crosssectional Study,” Verma et al, Journal of Clinical & Diagnostic Research . Dec2017, Vol. 11 Issue 12, p6-9. 4p.)
One can find articles on heart, bone, brain, etc. — studies that actually measure T3 levels, locally or in bloodstream–showing that low T3 contributes to disease.
I predict that soon the ATA will have to dismiss this growing number of studies on Low T3 and disease as irrelevant to the thyroid patient by categorizing them as studying “hypotriiodothyronemia” rather than “hypothyroidism.”
I’m telling you now, that’s going to be the next rhetorical sleight of hand, the next categorical fallacy, that arises from a fear of allowing T3 to usurp TSH in the realm of thyroid therapy.
Let the T3 paradigm continually point out that hypothyroidism is not a disease caused by hyperthyrotropinemia (high TSH). We do not have a pituitary secretion disorder.
Because hypothyroidism is NOT hyperthyrotropinemia, normalizing TSH by means of T4 monotherapy does not remove the cause of disease.
TSH normalization does not always “biochemically correct” hypothyroidism in organs and tissues outside of the pituitary gland that secretes TSH.
Back room ATA planning?
This is what I imagine overhearing in the back rooms of the ATA:
“Grumble grumble I guess we better do more research on T3/T4 therapy then…”
“We’ve got to reach out to these misled doctors who think they are being compassionate”
“We really need to show them once and for all that this renegade FAD of T3/T4 therapy does not work any better than T4 alone.”
“Here’s how we’ll do it. Let’s make sure all studies of T3-T4 therapy understand that
- They must never, ever use more than a 1:14 ratio of T3 to T4 even if we know that the thyroid gland does not have a static 1:14 ratio nor does its secretion always yield the same ratio of T3:T4 in blood or tissues.
- Patients’ subjective symptom relief must never be the goal of dose adjustments because it must be the primary, insignificant outcome we’re measuring for “success.”
- We must keep focusing on the patient as whiny and difficult, not truly unhealthy
- These studies must ensure that TSH is never, ever suppressed during the study, even if it means that patients are underdosed, or unable to achieve their optimal Free T3 levels in bloodstream, and therefore remain symptomatic.
“Once they play by OUR rules regarding the only ‘physiologically correct’ way to do T3/T4 combo therapy, these studies will fail to show any improvement in patient symptoms and health, and our choice of T4 monotherapy since the 1970s will be vindicated.”
Say no to rigged research studies
No, ATA, this is not how you use science to uncover truth that can heal patients. This is not about healing.
This is how you rig research studies so that an internal battle among endocrinologists and doctors, a war of medical ideologies, can be won.
This is not about finding truth, this is about generating statistics that will force practitioners to submit to the resulting skewed “evidence” — at the expense of patients!
The right way to do T4 monotherapy research
Before picking on what you call the “experimental” therapy, study your own human guinea pigs to be sure they are really healthy on your favorite “experimental” L-T4 monotherapy.
Do more studies on the long-term chronic low Free T3 levels of patients on LT4 monotherapy.
Follow patients who have maintained low Free T3 and see what their long term health outcomes are, even if they are not symptomatic.
Divide those patients into quartiles by their Free T3 levels and their T3/T4 ratios and their TSH, and then see what associations are found in each quartile.
No, do NOT exclude patients whose Free T4 or T3 is outside of reference range. You’re only allowed to exclude patients who don’t have a normalized TSH, since the normalized TSH is all you allow doctors to monitor in everyday real LT4 therapy. Normal patients don’t get to be excluded from taking Synthroid if their T4 goes too high or their T3 goes too low, because TSH is measured, and TSH alone, in long term monitoring.
No, do NOT be tempted to “adjust” your data to remove the statistical “confounder” of all other diseases just because you have a preconceived notion of the cause-effect direction with Low T3. I know, you may start out by believing that those other diseases are not caused by low T3, but rather, those diseases cause low T3. We charge you to keep an open mind and let the data speak for themselves about associations.
The right way to do T3/T4 combination therapy research
Now that you have done studies on your millions of human guinea pigs’ Free T3 levels and health associations, you must let the T3/T4 therapy people design their own study by THEIR OWN rules.
Let their therapeutic goals be what they ought to be if they truly care about resolving T3-based hypothyroidism and quality of life.
Let them define hypothyroidism as a suboptimal T3 in the presence of symptoms and/or signs of deficiency.
- Let these studies optimize Free T3 until hypothyroid symptoms disappear without causing any hyperthyroid symptoms, i.e. tachycardia
- Let these studies suppress TSH if and when necessary to achieve the goal above.
- Gather more than just Free T3, Free T4, TSH and subjective symptom surveys!
- Monitor not only all the potential adverse effects that could occur, but also the beneficial effects that could occur.
- Gather genetic data. Find out if they have DIO1 and DIO2 polymorphisms, TSHR, MCT10, and even partial SPB2 deficiency
- In the autoimmune patients, monitor their antibody levels. Measure TSH-receptor blocking antibodies that are present in atrophic thyroiditis patients
- Measure their thyroid gland volume and echogenicity to estimate functinoal thyroid gland capacity.
- Publish after 3 months, because we need data right away.
- Let the study continue after that for those that find benefit. Let it go on and on, and continue to generate research articles. If some patients elect to remain part of a longitudinal study and stay on this therapy that is working for them, keep the study going and publish results at 5 years. Are they sick? How about 10 years? Are they sick? How are their bones? their heart?