Why Do I Still Have All the Symptoms of Hypothyroidism?

Doctors and Current Treatment Approach are Keeping Many Thyroid Patients Sick

There are many reasons that some thyroid patients cannot get well. However, some thyroid patients are not allowed to get well.

In this blog post, I will discuss some of the significant issues holding back the recovery of some patients and leaving them with ongoing symptoms of hypothyroidism. 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.

So, let me start discussing some of the big issues that cause many thyroid patients to remain symptomatic.

The T3 thyroid hormone is not the main thyroid hormone focused on by doctors.

T3 thyroid hormone does almost all of the work for us all within our cells. T3 binds at the nuclear thyroid receptors. It is T3 that makes our cells run at the right rate. So, FT3 is the most important laboratory test to do. We know from research findings that it is ONLY FT3 that increases when symptoms improve.

Endocrinologists and doctors are not focused on the T3 level of their patients in a way that helps their patients get well. This is a massive issue. Currently, just being in range with TSH, and FT4 is all that is required for most doctors to think that their patients are well-treated. Even an FT3 result that is just inside the reference range, or mid-range, is thought by many doctors to be a good result. Some thyroid patients need their FT3 level to be higher. This is not a focus for most doctors. It is stopping the recovery of many thyroid patients.

T3 is just not understood as the most important thyroid hormone.

Thyroidectomy patients lose some T4 to T3 conversion ability.

Thyroidectomy patients often 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 important ability to convert T4 to T3. It can never be replaced with ‘additional conversion’ from other organs in the body. You cannot make T4 convert better than the body is doing it.  So, the loss of the thyroid in cases of thyroidectomy causes a serious loss of T4 to T3 conversion capability.

Note: this exact same situation occurs whenever the thyroid gland atrophies, e.g. in Atrophic Thyroiditis:
https://paulrobinsonthyroid.com/could-atrophic-thyroiditis-be-your-problem-it-is-not-always-about-hashimotos-thyroiditis/

Hashimoto’s thyroiditis patients also have conversion issues.

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 patient is also likely to become thyroid-less. So, Hashimoto’s thyroiditis patients also risk a serious loss of conversion capability. 

Atrophic Thyroiditis also has the same effect as it causes the thyroid gland to waste away.

Genetic reasons can play a part in poor T4 to T3 conversion.

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.

Laboratory test ranges are being used poorly by doctors.

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. The laboratory reference ranges are simply a guide and it is still essential to look at the clinical presentation of the patient.

This situation gets even worse when a thyroid patient is on thyroid medication that includes T3, e.g. T4/T3, NDT or even T3 Only. Laboratory reference ranges are created based on healthy people with no thyroid problems, or those patients on T4 Only medication. To even attempt to use the standard laboratory ranges for those on T3, laboratories would need to take a population of thyroid patients who are healthy on T3 and develop different ranges for these people. Shoehorning all thyroid patients to fit within the standard population ranges is extremely bad logic. It keeps a lot of thyroid patients who are on T3 sick!

TSH is being relied on far too much as an insight into thyroid hormones.

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.

Losing thyroid function leaves the thyroid patient deficient in T3.

In addition to the above, we know that when someone becomes ill with hypothyroidism, their entire thyroid system balance (homeostasis) is changed. The system does not work as well as it did in the past. The thyroid gland no longer steps in and keeps the level of Free T3 up to the level that is in a healthy person. On thyroid treatment, it is critical to ensure that the thyroid patient has enough T3 to correct their symptoms. Sadly, this usually does not happen. 

Other issues are frequently not looked at thoroughly.

Often other lab tests are either not done, or the results are said to be Ok when they are clearly too low, e.g. cortisol, ferritin, vitamin D, B12 etc. 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 are rarely at the forefront of doctors’ focus. Thyroid labs are just too easy to use instead!

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, and 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 is 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).

T4 monotherapy often fails to work but most doctors are not aware of this.

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 causing thyroid patients to continue to have symptoms of hypothyroidism. Here is a summary:

1. T4 to T3 conversion issues can affect a lot of thyroid patients to varying degrees. These have multiple possible causes.
2. The flawed application and interpretation of lab tests.
3. The flawed belief by most endocrinologists and doctors that the TSH-centric, lab-test-centric, and T4 monotherapy paradigm actually works.
4. The lack of focus on improvement in symptoms and signs as the main guide on whether the thyroid treatment is working
5. 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.

These issues are keeping some thyroid patients desperately ill.

Thyroid patients are not being allowed to get well because of current treatment practices!

Far too often the thyroid patient is left deficient in the active hormone FT3. When this happens a host of hypothyroid symptoms remain. Frequently, the thyroid patient has high blood pressure and high heart rate and their doctor even cites these as reasons for not increasing the thyroid medication or adding T3 to therapy. This is a mistake in so many cases because low FT3 causes cardiovascular stress and this can manifest as one or both of high blood pressure and high heart rate. I see this over and over again when I talk to thyroid patients and look at their lab test results.

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! 

Without a new paradigm of thyroid treatment thyroid patients will continue to ask the question, “Why do I still have all the symptoms of hypothyroidism?”

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). 

It is a disturbing situation but I hope that you found this article helpful.

Best wishes,

Paul