Why I Needed to Create CT3M and Why it Can be So Helpful
CT3M stands for Circadian T3 Method.
I created this approach 20-years ago, in order to raise my cortisol from a desperately low level to a healthy level.
It requires no use of hydrocortisone or adrenal glandulars to do this - just the use of T3 thyroid medication (liothyronine). For some people it can also work with natural desiccated thyroid (NDT).
Let me explain how I came to create (or discover) the Circadian T3 Method (CT3M).
I had been on T3-Only (with no T4 medication at all), for about 6 or 9 months and felt better in many ways. However, my low cortisol issue was still there.
Low cortisol showed up in my 8:00am morning blood test. On a 24-hour urinary cortisol collection, my total and free daily cortisol levels were near the bottom of the reference range.
However, I had passed a Synacthen test (ACTH Stimulation test), so my adrenals themselves were healthy. This latter situation is quite common with many thyroid patients, and I will return to this point.
In terms of low cortisol symptoms, my main ones were fatigue, low blood pressure, passing out (fainting) and weight loss. I was still so weak that I was virtually house-bound and had to spend a lot of my time laying down. The passing out instances became quite frequent and were linked to the low blood pressure.
For part of this time, I was struggling on in work and off work. Several times, I woke up in a corridor being looked at by worried colleagues.
My weight loss was severe. I had gone down from 170 pounds (12 stones or 76 kg) to 110 pounds (just under 8 stones or 50 kg), i.e. I had lost about 35% of my body weight. In contrast to most cases of poorly treated hypothyroidism, which causes weight gain, hypocortisolism can cause severe weight loss. I looked extremely ill.
I had been reading endocrinology books for a while and was aware of the pattern of FT3 over 24 hours, and the pattern of cortisol over 24 hours. I attach two charts showing these (these are straight out of medical literature, and this is knowledge that has been around for a very long time).
TSH is known to have larger and more frequent pulses in the night, and can be seen to peak around 3:00am in the morning. TSH is at its lowest in the afternoon.
FT3 is interesting too. FT3 peaks an hour or two after TSH peaks. It is also at its lowest in the middle of the day.
FT3 peaks in the night following the high point of TSH for two reasons:
- TSH drives a healthy thyroid gland to produce more T3 and more T4.
- We now know there is a connection between the TSH level and the rate of conversion of T4 to T3. When TSH is higher, the conversion rate of FT4 to FT3 increases. When TSH is lower, the conversion rate is lower. So, a high TSH in the night not only requests more T4 and T3 production from the thyroid gland, but it also increases the conversion rate of FT4 to FT3. Hence, FT3 increases in the middle of the night. In actual fact, TSH affects the regulation of the number of deiodinase enzymes being produced - which is why it effects the conversion rate of T4 to T3.
It should be immediately obvious that there isn't a huge variation in FT4 - it reduces slightly when there is more conversion to FT3, and it increases slightly when the conversion rate to FT3 reduces.
So, I knew all of this information already at this stage of my attempt to recover from hypothyroidism.
Looking at the cortisol rhythm, it is easy to see that cortisol begins rising around 3:00am and climbs to a peak between 7:00am and 9:00am in most people. This is to get us primed-up and ready to start the day. After this, cortisol normally declines steadily during the day, until the cycle repeats itself.
I knew my cortisol was very low and I was searching for an answer.
I was on T3-Only medication. At that time, I took 3 daily doses. One when I awoke in the morning, one around lunchtime and one in the late afternoon/early evening.
It occurred to me that, just like other thyroid patients, I was taking daytime thyroid medication. This tends to suppress the TSH, and the action of the thyroid gland (if someone still had a functioning thyroid gland at all).
The second thing that taking daytime thyroid medications tends to do, is to achieve good levels of thyroid hormone (FT3) in the daytime, but this FT3 is going to be lower during the night because we don't keep receiving the medication during the night. The use of daytime thyroid medication isn't a physiological replacement pattern at all. People on thyroid medication tend to have a lower TSH than healthy people have. Plus the normal, healthy pattern of FT3 is far less likely to be occur.
I had worked this much out but still hadn't understood why my cortisol was so desperately low. I was confused!
Then, one night, I just woke up around 3:00am and I had the answer. I had seen the connection - part of the answer lay in the two charts and their relationship.
We know from research that the pituitary gland has the highest concentration of FT3 in the body - more than any other organ or body tissue. The pituitary makes its own D2 deiodinase enzyme and uses it to convert the FT4 flowing through it to extra FT3. Much of this FT3 remains within the pituitary in order to keep its own T3 levels high. The pituitary gland runs on T3 - like a car runs on fuel!
The answer I had been searching for lay deep within the pituitary gland. If the pituitary was not receiving (or being able to create) the level of FT3 that it used to have, how could it function normally?
A person with lower FT3 levels than they had when they were healthy could easily have pituitary dysfunction. In this case, one of the pituitary hormones, like ACTH, could be lower than it used to be when the person was healthy. ACTH is the signal that drives the adrenal glands to make cortisol and Dhea. The adrenals usually perform well if they have enough cholesterol and an adequate ACTH signal. But without enough FT3 - all bets are off!
By the time I got up the following morning, I had the entire hypothesis worked out. I had low FT3 in the night time! This could be causing poor pituitary function and lower than adequate ACTH, thus low cortisol. I just had to test this hypothesis.
The following night I set my alarm to take my first T3 dose about 2 hours prior to my normal get out of bed time. I took it that coming night and I did feel a LOT better during the day. So, the next night I took it 3 hours before the time I usually got up. I felt better again! I was on to something here. This finally made sense.
I waited a couple of weeks to ensure that the improvement held - it did. I was elated. I went to see my family doctor. I explained it all - in fact I bombarded her with science and evidence. I then asked her if she would support me by allowing me to do multiple 24-hour urinary cortisol collections. She agreed! So, this started a 6-month long experiment.
I went back to daytime only dosing for a week and then did a 24-hour urinary cortisol collection. I then moved the first dose to 30 minutes before getting up and waited a week and then did another cortisol collection.
I repeated this process about 8 times. The last 2-3 tests were done by moving the first dose a full hour earlier. It was amazing that my doctor supported me. However, I'd been sick for so long and medically retired by my company at this stage and I was still extremely ill - so I think she was desperate for an answer too.
The results were INCREDIBLE.
Every time I moved the first dose earlier by 30 minutes, both total and free cortisol levels rose. I tested it to about 6 hours before getting up - to mirror the rise in natural FT3 rhythm. Once I got to about 4-5 hours prior to getting up there was no further benefit in taking it earlier, and it actually started to reduce the cortisol level beyond that. However, the correlation between the time the T3 was taken and both free and total cortisol levels was virtually linear. The earlier the dose, the more cortisol. It supported my hypothesis totally.
I began referring to the approach as the Circadian T3 Method or just CT3M.
I stuck with about 4 hours before getting up time for my CT3M dose. I got an immediate benefit from CT3M and it enabled me to begin to function quite well again. I even began to exercise and started on the long road to recover my fitness. Over the following few years, my cortisol slowly improved. I have been using CT3M for many years now. If I try to not use it, my cortisol levels lower and I feel unwell.
I have also discovered, in the past year, that I have both copies of the DIO1 and DIO2 gene defects. DIO2 can impact the production of effective D2 enzymes. Thus, this could also have impacted my pituitary and its abilty to convert FT4 to FT3, when on T4 and NDT medication. By the time I was on T3-Only during the daytime, it was the strictly daytime use of T3-Only that was the issue.
I published 'Recovering with T3' in 2011. The majority of this book is about the safe and effective use of T3-Only and the protocol for doing that. Only a small part of it introduced CT3M and its potential benefits to those with low cortisol. It included a protocol for starting CT3M, and determining the correct CT3M dose size and timing.
In 2013, I published 'The CT3M Handbook', with more information on using CT3M. I have worked with thousands of thyroid patients now and many of them have also improved their cortisol levels using CT3M. Some have regained their lives in dramatic ways through using it. It can work with NDT in some cases, but T3 works best. However, a T3 CT3M dose and daytime NDT is something that thyroid patients opt for quite often.
These days, I have really changed my views on what I think causes low cortisol in most cases. I no longer believe in the concept of Adrenal Fatigue. I do not believe that the adrenals get tired at all. If they could get tired, then those with Cushing's disease would not be able to have super-high cortisol levels for years. I actually believe that most cases of low cortisol are caused by hypothalamic-pituitary dysfunction and the lower than normal ACTH signal that goes with this. Sometimes, there is no known cause for this, and yes, stress could well be a factor. In some cases, the low cortisol is due to the way we use thyroid meds and the fact that this is not physiological. In these cases, CT3M can bring about profound improvements in cortisol levels throughout the day. Results with many thyroid patients have shown how worthwhile a trial of CT3M can be.
It is a shame that so many thyroid patients who are taking T4, NDT or T3 medication are sometimes persuaded to use hydrocortisone or adrenal glandulars to 'top up' their cortisol levels. This often does not work well, as the added cortisol in these medications simply causes the pituitary gland to produce even less ACTH, and the patient's own adrenals produce less cortisol. This frequently leads to the dependence on a full replacement dose of cortisol and the issues associated with this (needing to carry stress doses, needing to carry some kind of medical bracelet or medallion in case of emergency hospitalisation etc.). CT3M is often worth a trial first before going down these routes. In many cases, CT3M raises cortisol right across the day. In some cases, it does not work as well or at all, depending on the severity/nature of the hypothalamic-pituitary axis issue. In a few cases, the issue is actual adrenal damage - but this is far more rare.
So, this is a little more background on CT3M. It explains how I came to discover it and why it can be so amazingly helpful.
I believe that the connection between T3 thyroid hormone and cortisol ought to be part of mainstream endocrinology.
I also think that CT3M ought to be in the 'toolbox' of every endocrinologist or doctor who is dealing with thyroid and cortisol issues.
I hope that you found this interesting.