No, just make the switch. Honestly, I don’t think you will get much out of thyroid meds with your levels, but it’s worth a try.
Take the meds fasted and don’t eat until 1-2 hours after taking them. And especially don’t take any vitamins with minerals in them until 8 hours or so after the meds. They will stunt the absorption of the medication.
It can take a couple months to really feel a difference. T4 is a slow acting medication. T3 is much faster, so you might feel better fairly quickly on the NDT.
I’d also recommend splitting your dose into twice a day, since the T3 Elimination half life is only about 8 hours.
And when i switch to NDT what will be the best time to take supplements? I mean i take dozens of stuff. Vitamin D, C , B complex , Mag , Copper , Zinc , NAC , Glutamine etc… I don’t take them all at once either. Many minerals are antagonists so i have to take them 2 hours apart from each other.
8 hours is probably excessive. It’s just what I do because it fits my schedule. Thyroid in the am and vitamins before bed. I’d just take them as far apart as makes sense with your schedule.
Honestly with a good diet you shouldn’t need all those supps, waste of money. Maybe just magnesium before bed for the sleep benefits, and definitely keep the vitamin D.
I’d try quitting caffeine for 2 months and see what happens. Quitting caffeine made a profound difference for me, even more so than TRT did. Results may vary, but also worth a try.
Yes switch to dessicated thyroid like armour thyroid. It’s the best.
Your ft3 levels are rock bottom. You need to get in a good dose right away. I would guess you’ll end up at 1.5 to 2 grains am and again at pm. 8 hours apart on an empty stomach.
I highly doubt 1 grain will work welll with such low levels. Might be wrong, but I highly doubt it.
Reverse t3 is also a bit higher. If you take armour thyroid and don’t feel better you might need to start t3 only and lower the Rt3. You do this by eating health carb to protein ratio. Don’t cut down carbs and cortisol also plays a role. Do some research and you’ll find many more reasons.
You can lower that reverset3 in 1-2 months if your diet is the cause, (like keto)And you fix that diet By going back to carbs. You get the idea.
I would want my Rt3 below 5, but I would start armour around 6-7ish.
T4 converts to Rt3 if you don’t fix the issue and it will only make it worse. So make sure whatever is causing Rt3 to be high is tackled ASAP.
I thought we were talking about t3. Also you do realize the t4 is what builds up and the t3 is what would work right away. Therefore I am mostly correct . Within hours his issues should resolve. As long as he didn’t continue taking his dose for days after symptoms appeared.
@galgenstrick doubts i will benefit from thyroid meds at all and thinks 1/4 grains of Armour will be enough and you think 1 grain won’t even be enough … I am confused I will def. let you guys know the outcome but i think it will be wise to start with 1 grain at least.
For that people tend to go for the T3 only route right? My RT3 labs is a rollercoaster… It can be 11.4 , next month can be 17.0 and the other month might be 13.0… But never single digits…
I did alot of reading for RT3 and some think it’s necessary to bring it down and some think the opposite… I think i will see it myself within few weeks…
I eat healthy/quality carbs everyday… Never did keto… My iron panel is on point too… So not sure what causes my high RT3.
You mean i shouldn’t start Armour before i bring it down to 5? The reference range 9 - 21.5 ng/dL though.
I was referring to a conversion chart for grains. I think I might have been reading the chart wrong. It looked like 1 grain was equivalent to 100mcg T4 and 25mcg of T3. But I just saw the bottom of the chart stated 1grain is 38mcg T4 and 9mcg of T3. If that is true, then 1/4 grain is not enough. You would probably need to be closer to 3/4 - 1 grain.
@highpull A follow up on this. I’ve dialed in testosterone dose and started 25 mg of DHEA as you suggested in the other thread. The latter has helped with mood and getting better sleep, and I’m going to re-test Thursday to see how the values has changed and I’ll pull a full thyroid panel again, as I want to see if I can finally solve the brain fog and memory issue that have been persecuting me recently with some thyroid meds.
I’m back in Europe so I have access to a proper compounding pharmacy through prescriptions. I just wanted to understand if by compounded T3/T4 you mean synthetic T3 and T4 or natural dessicated thyroid. I have access to both through the compounding pharmacy, but I think I prefer the natural bio-identical version. Just wanted to know your thoughts before ordering.
Last thing. rT3 was 13 last time I checked, but I will test it again on Thursday as I said before. If rT3 goes up significantly with a combo of T4/T3, what do you do? Introduce more T3 in a second daily administration, or go on a T3 only administration multiple times per day?
Thanks.
I’m 191 pounds 11% bf at the moment, that I will bring down to 10% in a couple of weeks.
Should I start on 22/145 mcg as you said months ago? A single dose in the AM?
Doctors are clueless here. They prescribe euthyrox and walk you out the door.
I’ve basically found a doctor who was able to listen and understood that I did my homework.
So he let me experiment with things, as far as I do regular blood work.
I introduce one thing at a time and test the outcome with blood tests and assess how I feel.
Thyroid is the last thing left to optimize and I’m trying to see if it gets rid of brain fog once it reaches optimal levels.
The dose above seems to be the equivalent of 2.5 grains for T3 and almost 4 grains for T4. Too much as a staring dose?
Wait, I’m introducing T4 and T3, not only T3, so why should T4 go below range?
I understand your appreciation for dr. Saya and while I agree with you on the human side, he kept me symptomatic with a Free T of 25, that was really good according to him, while I started feeling better only when I went above 30 and total T above 1000 ng/dL.
The conservative approach you and Dr. Saya are preaching now was my belief as well, but 800-900 ng/dL of total T never did anything to me in terms of symptoms resolution, especially when paired with “a really low dose of AI”, due to E2 fear mongering.
Also, I would like to know your opinion regarding my numbers, since TSH has reached 3.6 and that would be considered hypothyroidism, according to the new guidelines in the US.
Also, as a refusal of your statement, you may want to read this meta-analysis that report both sides of the T3/T4 debate:
In mammals, the majority of active thyroid hormone (T3) within cells is derived not directly from T3 in the circulation, but indirectly from T4, via the action of the D2 deiodinase (29, 30). The concentration of circulating T4 is about five times higher than T3 and it is the circulating T4 rather than T3 that serves as the main source of thyroid hormone for the body (5). In addition a proportion of serum T3 is also derived from serum T4 (5). These considerations have been used as a key theoretical argument against the use of LT3 in the management of hypothyroidism.
However, serum thyroid hormone levels may not entirely reflect intracellular thyroid hormone status. Via variation in uptake, activation and metabolism of T4, cells can modulate intracellular T3 levels independently of circulating thyroid hormone levels. Downstream control by thyroid hormone transporters such as MCT8 and MCT10, the deiodinases (DIO2,DIO3), and transcription co-factors locally modify thyroid hormone bioavailability and action at the intracellular level. The potential for dichotomy between serum thyroid hormone levels and intracellular action is dramatically illustrated in reports of individuals with rare mutations in the MCT8 transporter (Allan-Herndon-Dudley syndrome) or the thyroid hormone receptor alpha (present in many tissues but not the hypothalamus/pituitary) (31, 32). Here, marked tissue-specific hypothyroidism is seen with dramatic effects on bone and brain development despite “normal” or even raised serum thyroid hormone levels (31, 32). The effects of more common variants are less clear.
At the same time evidence has been accumulating of tissue-specific regulation of thyroid hormone contents in tissues via differential expression of thyroid hormone transporters and iodothyronine deiodinases (29, 33). It has been hypothesized that LT4 monotherapy may not restore intracellular T3 levels in the brain in all patients and this may explain the dissatisfaction some patients have on LT4.