T3 Treatment and CT3M – Their Relevance in Thyroid Treatment and Other Conditions

I know from personal experience and from dealing with thousands of thyroid patients over a 10 year+ timescale that T4/T3 combination therapy (including the use of natural desiccated thyroid) is often required. Some thyroid patients need T3-Only therapy. All the treatment options need to be available for every doctor to choose from when dealing with individual cases. In some cases, the Circadian T3 Method (CT3M) is also required in order to raise cortisol levels.

Every thyroid patient is different. We are not all the same in the way our systems work and do not work. Some thyroid patients have lost thyroid tissue (through thyroidectomy or Hashimoto’s) – this loses around 25% of their T3, mostly through the loss of T4 to T3 conversion capability. Other thyroid patients have poor conversion ability due to deiodinase enzyme production defects in their genetic makeup (DIO1 and DIO2 gene defects). See my blog post on this: https://paulrobinsonthyroid.com/dio1-and-dio2-gene-defects-and-testing-them/

T3 stimulates every tissue and organ to do what it does. It is critical for energy production in every organ. This includes the hypothalamic-pituitary (HP) system. Low thyroid effect in the HP system reduces all hormones. This is why hypothyroidism is in the differential diagnosis (what doctors should consider as an alternative diagnosis) in cases of testosterone deficiency, amenorrhea, growth hormone deficiency, and hypocortisolism.

T3 in T4/T3 combination therapy and especially in T3-Only therapy often manages to raise cortisol from a low level to a normal level. This sometimes requires the use of my Circadian T3 Method (CT3M) protocol (defined in the Recovering with T3 book, and in The CT3M Handbook). I have seen this many times in thyroid patients being treated with T3. Research studies make it clear that the pituitary is known to have the highest concentration of T3 within its cells compared to other tissue in the body. The pituitary produces its own D2 deiodinase enzymes and is a prolific converter of T4 to T3. So, in a healthy person with good conversion, the pituitary basically runs on T3, as its fuel.

In the Recovering with T3 book, I describe what I did to raise my own cortisol level from dreadfully low to normal using CT3M. I discovered that taking T3 several hours before people get up in the morning helps the pituitary to produce the high early morning levels of ACTH and get morning cortisol back up to normal.

This is why I think that T3 use could be instrumental not only for thyroid patients who remain with severe symptoms of hypothyroidism when on T4-monotherapy but also for patients suffering from conditions like fibromyalgia, chronic fatigue syndrome (CFS) and ME. I believe in many of those conditions the problem is the hypothalamic-pituitary (HP) system that is no longer ensuring the end hormones are produced at a good enough level.  This is especially true if patients with these conditions have low cortisol.

The T4 hormone does virtually nothing. It has effects only if it is converted to T3 (in healthy people who are good converters of T4 to T3). If T4 monotherapy does not work well and results in lower levels of T3 production than in a healthy person, then T3 needs to be used either in combination therapy or on its own in T3-Only treatment.

I believe that T3 ought to be one of the options available when treating conditions like CFS, ME, and fibromyalgia (where end hormones like cortisol and T3 are often lower than ideal).

Higher T3 levels stimulate ACTH and cortisol production, and other end-hormones modulated by the HP system.  In hypothyroidism, ACTH and cortisol production is often reduced significantly even to the point to suggest there is a pituitary problem.

In summary, T3 therapy, and CT3M, should be an option for thyroid patients who do not respond well to other treatments. These treatments also should be an option for CFS, ME, and Fibromyalgia patients who need to have their hypothalamic-pituitary system given a boost up. T3 is about the easiest way to help the HP system.

Here are some research references:

1. Sánchez-Franco F, Fernández L, Fernández G, Cacicedo L. – Thyroid hormone action on ACTH secretion. Horm Metab Res. 1989;21(10):550-552.
The Abstract is here: https://www.ncbi.nlm.nih.gov/pubmed/2553572
This paper clearly provides actual research backing for why the Circadian T3 Method (CT3M) works so well. By providing the hypothalamic-pituitary system with enough T3 when it needs to drive ACTH high, CT3M helps to raise morning cortisol to normal levels.

2. Lizcano F, Rodríguez JS. Thyroid hormone therapy modulates hypothalamo-pituitary-adrenal axis. Endocr J. 2011;58(2):137-142.
The abstract may be found here:

3. Bigos ST, Ridgway EC, Kourides IA, Maloof F. Spectrum of pituitary alterations with mild and severe thyroid impairment. J Clin Endocrinol Metab. 1978;46(2):317-325. The abstract may be found here:

4.Tunbridge WM, Marshall JC, Burke CW. Primary hypothyroidism presenting as pituitary failure. Br Med J. 1973;1(5846):153-154.
The abstract and full text are available here:

5. Paula Bargi-Souza · Rodrigo Antonio Peliciari-Garcia · Maria Tereza Nunes.  Disruption of the Pituitary Circadian Clock Induced by Hypothyroidism and Hyperthyroidism: Consequences on Daily Pituitary Hormone Expression Profiles. Thyroid. 2019 Apr;29(4):502-512.
doi: 10.1089/thy.2018.0578. Epub 2019 Mar 13.
The abstract is:  https://www.ncbi.nlm.nih.gov/pubmed/30747053

I hope you found this interesting.

Best wishes,


Paul Robinson

Paul Robinson is a British author and thyroid patient advocate. The focus of his books and work is on helping patients recover from hypothyroidism. Paul has accumulated a wealth of knowledge on thyroid and adrenal dysfunction and their treatment. His three books cover all of this.

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