There are many reasons that some thyroid patients cannot get well. However, some thyroid patients are not being allowed to get well.
In this blog post, I will discuss some of the significant issues holding back the recovery of some patients. I am not going to discuss other conditions and deficiencies, as this would make this article far too long and less readable. Much has already been written about ‘other issues’ on this blog and I discuss many of the main ones in The Thyroid Patient’s Manual.
Thyroidectomy patients lose about 25% of their T3 production. Most of this loss comes from the T4 to T3 conversion that the thyroid is responsible for, not the T3 it produces. The thyroid gland is the most important converter of T4 to T3 in the body (more important than the liver). The thyroid gland uses both D1 and D2 deiodinase enzymes in order to convert the T4 flowing in the bloodstream to T3. It is like a ‘little machine’ in the blood flow that converts T4 to the active hormone T3. So, the loss of the thyroid gland means the permanent loss of that ability to convert T4 to T3. It can never be replaced with ‘additional conversion’. T4 does not do this. You cannot make T4 convert better than the body is doing it. In addition to this, thyroid cancer patients who have a thyroidectomy are often on TSH suppressive doses of T4 (Synthroid or Levothyroxine). So, the loss of the thyroid in cases of thyroidectomy causes a serious loss of T4 to T3 conversion capability.
Hashimoto’s thyroiditis patients also lose thyroid tissue. Over time, unless the autoimmune response can be halted, the same thing will happen to them as in thyroidectomy patients! They are just on a sliding scale with respect to T4 to T3 conversion loss from the thyroid gland vs. a total loss with thyroidectomy. After many years a Hashimoto’s patient is also likely to become thyroid-less. Hashimoto’s thyroiditis patients also risk a serious loss of conversion capability.
The DIO1 and DIO2 gene defects affect the ability of our cells to make good, effective D1 and D2 deiodinase enzymes. There are two copies of each gene – one from each parent. If someone has only one bad copy (gene defect) and one good copy, they are said to be heterozygous for the gene defect. If they have both bad copies they are homozygous. This applies to both the DIO1 and DIO2 genes. The gene defects often do not manifest until someone is in their late twenties or early thirties. If these gene defects do appear to be causing issues the homozygous situation (both copies of each gene defect) is usually more serious. DIO2 is also more serious, as the D2 enzyme converts T4 to T3 more efficiently than D1. Having both D1 and D2 defects is also worse of course. So, these gene defects can seriously affect the ability of someone to recover on T4 medication.
Lab ranges are the side of a barn door! I have discussed this before:
The lab ranges are wide population ranges and have little resemblance to the range an individual’s FT4 and FT3 need to be in for them to feel well. Lab ranges are not ‘normal ranges’. The way lab test results and lab reference ranges are being used today is leaving many thyroid patients inadequately treated. We do not know where an individual’s own personal ranges are. So, the wide population ranges are not useful for fine-tuning a thyroid patient’s medication. We know from medical research that an individual’s ranges are less than half as wide as the population ranges used for thyroid testing.
TSH itself is also no measure of thyroid hormone action. It is profoundly misleading and research has proven that the movement of TSH under thyroid treatment does not track the patient’s symptoms at all.
In addition to the above, we know that when someone becomes ill with hypothyroidism, their entire thyroid system balance (homeostasis) is changed and it does not work as well as it did in the past. Often the level of FT3 that a thyroid patient needs is higher than a healthy person. It is an entirely different situation to have hypothyroidism and be under treatment for it, to the situation prior to developing hypothyroidism.
Often other lab tests are either not done, or the results are said to be Ok when they are clearly too low, e.g. ferritin, B12. Other issues are thus not diagnosed or ignored.
There are of course many other issues that can impact thyroid hormone action and the above is by no means attempting to be complete.
Symptoms and signs need to be centre-stage – they do indicate how thyroid treatment is working. Symptoms might include energy level/fatigue, feeling cold/warm etc. Signs might include body temperature, heart rate.
Symptoms and signs show the actual response of the body, whereas blood test results just show what is in the blood. The latter made worse by comparing the individual’s results to a wide population range.
Unfortunately, symptoms and signs are looked at as less important than TSH and other thyroid lab tests (if others are even done).
We are also in a seriously messed up situation where most endocrinologists and doctors believe that T4 monotherapy works well for all thyroid patients. T4-Only cannot work well for the many patients who have lost T4 to T3 conversion capability (this is without even looking at all the many other issues that can cause issues with T4-Only and impact thyroid hormone action).
So, there are many issues that include:
- Many reasons why thyroid patients might be having conversion issues.
- The flawed application/interpretation of lab tests.
- The flawed belief by most endocrinologists and doctors that the TSH-centric, lab-test-centric and T4 monotherapy paradigm works.
- The lack of focus on symptoms and signs as the most important thing to improve.
- The near-total disbelief that T3 in combination with T4, or NDT or in a few cases T3-Only, is needed at all. In many parts of the world, T3 is being refused and thought to be unnecessary.
All of the above issues (and others) are keeping many thyroid patients from recovering.
For some thyroid patients, these issues are keeping thyroid patients desperately ill.
Thyroid patients are not being allowed to get well because of current treatment practices!
It is time to accept the new research findings and embrace a new treatment paradigm (approach) that will actually work.
The research findings are already out there to show how treatment needs to change.
Past clinical trials are flawed but randomised clinical trials (RCTs) are not the best way to prove treatment anyway. The FDA in the US relies far more on experience with medication in a clinical setting, where doctors are able to use clinical experience to the best extent in utilising medications.
There is plenty of clinical evidence for the need for all the treatments to be available already. T4 monotherapy will not make everyone well – ever!
We need to have all the thyroid treatments available and we need a sound approach to the use of clinical presentation and thyroid labs during treatment.
It is absolutely necessary at this time to renew the paradigm and move forward!
All the above is discussed in my latest book The Thyroid Patient’s Manual, as is the correct use of thyroid labs and the correct use of all the different therapies (T4, T4/T3, NDT, and T3-Only).
I hope you found this useful. It is disturbing but hopefully helpful.