T3 Thyroid Hormone and Cortisol Relationships Summary

I was asked recently to explain my views on the relationship of the T3 thyroid hormone to Cortisol. This is an easy question to ask but an extremely complex one to answer.  It is difficult to answer questions like this in an email or on a forum and provide a good enough understanding in order for the person to make really good decisions.

My books are definitely the best source of information that I have to offer to thyroid patients about the relationships between T3 and Cortisol.

I write about this topic extensively in all three of my books:
The Thyroid Patient’s Manual, Recovering with T3 and The CT3M Handbook.

My website blog also has numerous articles that cover various aspects of this subject and it is very searchable. I recommend searching for any word or phrase that you think might be relevant to what you are interested in, e.g. ‘cortisol’, CT3M’, ‘T3 and cortisol’ etc.

However, I have received numerous requests for a brief summary of the important relationships between T3 thyroid hormone and Cortisol. I have put these in bullet point form in this blog post.

Some important T3 thyroid hormone and Cortisol relationships:

1) Cortisol and T3 are partners. T3 and Cortisol both need to be at good levels. Cortisol increases T3-effect, and T3 increases cortisol-effect – they are in a partnership within the cells. They both work at the mitochondria and at the cell nuclei. In addition, one of cortisol’s roles is glucogenesis. This converts stored sugars into available sugar in the bloodstream in between meals. Glucose (blood sugar) is needed by the mitochondria in order to produce cellular energy (ATP). Assessing glucose levels is an indirect way of assessing cortisol levels. It is not the most definitive way, but it can help when trying to get cortisol optimal.

2) The pituitary gland controls cortisol production via the Adrenocorticotropic Hormone (ACTH).  ACTH stimulates the adrenal glands to produce both cortisol and Dhea. Without enough ACTH, cortisol production by the adrenals will be too low.

3) However, studies show that the pituitary gland needs more T3 than any other organ in the body. The pituitary basically runs using T3 as its fuel. This makes the pituitary vulnerable to not working well if T3 is low.  This is fundamentally why low cortisol is so prevalent in thyroid patients. Many thyroid patients are on treatments that do not give them sufficiently good T3 levels. It is such an obvious conclusion. Poorly treated hypothyroidism (low T3 levels), often results in low cortisol.

4) Adrenal Fatigue is a bit of a myth. Adrenals do not usually get ‘tired’ or ‘overworked” unless they are damaged by disease or autoimmune attack – i.e. Addison’s disease.  Usually, the issue is the lack of enough pituitary signal (ACTH).

5) The pituitary can fail to produce sufficient ACTH signal to the adrenal glands because of hypopituitarism (which can be tested for) or simply because it is not receiving enough T3 thyroid hormone (see point 3). Many other issues can cause the hypothalamic-pituitary (HP) system to fail to regulate the adrenal glands with sufficient ACTH at all times over the day.

6) T3 is more likely to stimulate cortisol production than T4. T3 helps to keep cortisol levels up as it stimulates the hypothalamic-pituitary system more than T4. This latter point is why thyroid medications that contain T3 often help to keep cortisol levels higher.

7) Low cortisol is very common in thyroid patients, as many have lower T3 levels than they had when they were well (for reasons I have discussed in my books and in various other blog posts).

8) Cortisol is not required for T3 to be able to enter the cells. T3 enters our cells through transporter molecules and these do not require cortisol to function. Therefore, there is no evidence that low cortisol causes T3 ‘pooling’ or ‘build-up’ or inability to enter our cells. In fact, new research as of 2021 proves the opposite is true – high levels of cortisol actually inhibit T3 transport into the cells, whereas low levels do not. The idea of ‘pooling’ is simply another Internet myth that is incorrect and misleading. See this blog post for more details, including a reference to the new research:

9) Low cortisol causes T3 to work less effectively within the cells. This is because T3 and cortisol are partners within our cells. High cortisol also causes problems and can reduce the effectiveness of T3 within the cells, hence thyroid patients with high cortisol often complain of feeling hypothyroid even when they appear to have reasonable FT3 levels.

10) When patients try to raise T3 levels in the presence of low cortisol, they may find that the body compensates for low cortisol by producing more adrenaline. This can cause anxiety, rapid heart rate, the feeling of heart palpitations etc. This is usually the adrenaline response rather than a direct issue with the T3. Very often, it is the low cortisol that is at the root.

11) When cortisol is low, taking daytime T3 is often enough to correct it. However, it sometimes also needs nighttime dosing of T3. See my Circadian T3 Method (CT3M) protocol in the Recovering with T3 book. CT3M is also covered to some extent in The Thyroid Patient’s Manual and in detail in The CT3M Handbook.

12) Cortisol dysfunction patterns are numerous. Often there is low in the morning, rising to high in the evening due to the pituitary being very slow to catch up. Sometimes there is low all day. Sometimes there is high cortisol due to the strain of low T3 and high rT3. In many cases, if the person is hypo, getting the T3 levels up without high rT3 can help. Sometimes it needs CT3M. CT3M can help with many patterns of cortisol dysfunction – not just low morning cortisol.

13) Low cortisol is a serious issue for thyroid patients. It is important to rule out Addison’s disease by having the appropriate ACTH Stimulation test done (also known as a Synacthen test). This can only be done under the supervision of a qualified endocrinologist. Addison’s disease can be life-threatening and any thyroid patient with low cortisol needs to have this tested for and ruled out.

14) If Addison’s disease is diagnosed then cortisol will need to be replaced and this is likely to be a life-long requirement. This should be done under the supervision of an experienced endocrinologist. There are many alternative medications and approaches to cortisol replacement. If one solution does not work, another may be tried. Some endocrinologists are far more experienced with various solutions for cortisol replacement than others. So, finding a specialist who is knowledgeable and experienced is very important when cortisol replacement is needed.

15) Some Addison’s disease patients are finding that when cortisol replacement is needed that only a cortisol pump replaces cortisol in a physiological way. Search my website for ‘cortisol pump’ to find out more. Replacement with cortisol is a serious step and it does need an extremely competent endocrinologist to help with this.

16) Hypopituitarism can also result in an insufficient ACTH signal to the adrenal glands. This too may be tested for (see The Thyroid Patient’s Manual book for some of the possible tests). There are various tests for hypopituitarism and these can also be organised by a competent endocrinologist. If hypopituitarism is present then replacement of cortisol is also likely – see points 13 and 14.

17) However, most causes of low cortisol are not as serious as Addison’s disease or hypopituitarism. Correcting hypothyroidism may frequently resolve any low cortisol issues. Hence the need to be aware of the potential connections between T3 and cortisol.

18) Many thyroid patients who have low cortisol, or have the symptoms of low cortisol, are often persuaded to try to raise cortisol by various methods. Some are told that herbs known as Adrenal Adaptogens will work. However, these often lower cortisol levels (herbs do not have brains – herbs cannot work out whether to raise or lower cortisol for the individual). Some patients are persuaded by doctors or other patients to try to use either hydrocortisone (bio-identical cortisol) or adrenal cortex extract from animals. These types of approaches are a mistake if the problems are really connected to low T3 levels or some other issue that needs to be addressed, e.g. low B12, low iron etc. I would always want to explore other solutions for low cortisol before resorting to any form of cortisol replacement, as this switches off the individual’s own cortisol production ability.

Finally, I emphasise again that The Thyroid Patient’s Manual book is a good starting point to learn about the thyroid hormone and cortisol systems. Recovering with T3 is next and covers the safe use of T3 and of CT3M if it is required. My website blog is very searchable and useful too:

I would advise against relying mainly on Internet forums – mine included. Building a more comprehensive knowledge base is always the best thing to do. Once you understand how the important systems of the body actually work, then it is possible to make sense of things. Hence, I recommend reading my books. Clearly, finding a knowledgeable doctor or endocrinologist that you can work well with can be very important to regaining your health. Be prepared to switch doctors, or keep looking for someone who you can work with – it can help a great deal.

I hope this is helpful.

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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  1. Sandra on 11th April 2022 at 9:01 pm

    Hi Paul, Do you happen to have any articles/insights re: 1. undiagnosed or untreated ‘subclinical’ hypothyroidism (3.4 TSH) and how this effects menopause, and, 2. the effects of low FT3/mid-low FT4 on blood sugar regulation? 2 years into menopause. When I started using bi-est 1.25 with 20mg progesterone so many symptoms resolved except I felt cold all the time. When I stopped using BHRT for a dexa challenge to test cortisol because morning blood sugar was high despite a 5.4 A1C, I had high or 3 points above range morning cortisol. This is in part explained by hypoglycemia episodes as I wear a CGM to track. Interestingly, or not, I had a strange reaction to dexa 1 hour after taking it i.e. woke from sleep with a severe anxiety-like attack. MD said this wasn’t of concern. I re-started BHRT thinking this was needed due to brain fog and lack of energy/motivation (working professional), inability to lose weight despite focused effort on diet and exercise to do so, worsening fasting glucose, and now my cortisol appears to be on the low end based on low blood pressure and BHRT isn’t improving any symptoms. So, on a hunch, based on historic lab results for TSH: 1.8 / 2.6 / 3.4 (progressively worse) I am trying NDT and feel better, warmer via checking temps, severe nail ridges on hands and feet are going away, eye puffiness going away. Curious, does menopause without using hormone replacement ‘unmask’ hypothyroidism? Is hypothyroidism the real culprit behind why some women have such a difficult time in menopause vs. others? Love your comment re: adaptogen herbs…they don’t have a brain!

    • Paul Robinson on 12th April 2022 at 9:33 am

      Hi Sandra,
      Having hypothyroidism won’t help someone who has sex hormones that are already too low during menopause. It is unlikely to be the reason for going into menopause but it certainly won’t help.
      All I have to say on this subject is contained in a chapter in my The Thyroid Patient’s Manual book plus in this blog post you have commented on.
      I haven’t got any other links, sorry.
      Best wishes, Paul

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