The Flawed Concept of 'Resting Adrenals'

So much has been written on the subject of 'resting the adrenal glands' when a thyroid patient is suffering from low cortisol. The idea is to use hydrocortisone (HC) or adrenal glandulars in order to 'take the strain off the adrenal glands' and 'rest them'.

It is based on the idea of 'adrenal fatigue', i.e. the the adrenal glands have got tired of making cortisol and that is why it is now the patient now has low cortisol.

I no longer believe in 'adrenal fatigue'. The adrenals are very simple glands with ample capability of producing high levels of cortisol, indefinitely. All they need is a good ACTH signal from the pituitary and adequate cholesterol. 
ACTH is adrenocorticotropic hormone and it stimulates the adrenal glands to make more cortisol and Dhea.

The above goes a long way to explaining why people with Cushing's syndrome can go for years and years with extremely high cortisol levels - their adrenal glands do not get 'fatigued'. 

I believe the majority of cases of low cortisol are due to hypothalamic-pituitary dysfunction, or HP dysfunction and the lower level of ACTH that results from it. 

Of course there are some cases of Addison's disease, which can be discovered fairly quickly via an ACTH Stimulation test (Synacthen test).  Addison's disease is caused through adrenal tissue destruction, often through auto-immune attack. It requires hydrocortisone (HC) replacement for life.

But for the typical thyroid patient with low cortisol, it is likely to be HP dysfunction causing the low cortisol. Many things can cause this e.g. prolonged stress, toxicity etc. The result is the same - low cortisol. 

Sometimes the cause for the HP dysfunction cannot be discovered and the patient may require some HC, or adrenal glandular support.

However, it is often caused by the use of thyroid medication.

Why Can the Use of Thyroid Medication Cause HP Dysfunction?

The pituitary has the highest concentration of free T3 (FT3) in the body. It also makes its own D2 deiodinase enzyme. It converts around 80% of the FT4 present in its cells to FT3 and it keeps the T3 there. Why? It needs a good supply of FT3 to function well of course. If anything lowers FT3, e.g. a conversion problem, the pituitary will suffer and ACTH could be lower. 

With lower ACTH comes low cortisol.

What can cause a lower level of T3 in the pituitary gland? Factors include: Hashimoto's thyroiditis, thyroidectomy, a DIO1 and especially a DIO2 enzyme defect (which affects internal pituitary conversion of T4 to T3), or anything else which lowers T3 levels. Taking thyroid medication in the daytime only, is also likely to lead to lower levels of FT3 by the night time when the pituitary begins to crank out a lot more ACTH.

Treating HP-dysfunction with levothyroxine or Synthroid is often not going to work. It  needs extra T3 to bring the system back to normal. In some cases it needs T3-Only.

'Resting the adrenals' with steroids is a fallacy. The adrenals won't miraculously recover, as there is usually nothing wrong with them to begin with.

It needs a better, smarter approach.

Using more T3, and the Circadian T3 Method (CT3M) can often help resolve the HP-dysfunction and raise cortisol levels back to normal. 

See the following link for more information on CT3M: http://recoveringwitht3.com/blog/what-circadian-t3-method

For those that want to dig deeper into CT3M, please read 'Recovering with T3'.

A companion book, 'The CT3M Handbook', is also available if you need even more information on CT3M.

Best wishes,

Paul

(Udated in February 2019)