Does anyone use both, and do you top up with t3 to symptoms as discussed, for example on STTM? Would really like to hear other people's experiences of what does or doesn't work for them.
At the moment I'm finding that my ND runs down by the afternoon and I top up with t3 to relieve hypo symptoms. I feel OK on the longer lasting effect of the NDT but I'm struggling to raise NDT for a longer lasting therapy as I feel over stimulated quite quickly and finding it easier to control symptoms with t3 and a lower dose of NDT. Maybe I just need to bite the bullet and add another NDT dose but I feel it sneakily gathers up on me and dumps when I least expect it. The lower dose of NDT does feels OK for about 6 - 7 hours then I slump, then control the deficit with small doses of t3 to symptoms. The careful multi dosing is a pain but I am experiencing better control over the short term as opposed to a wallop from the NDT. I did try t3 only but not for long enough...I think I am a bit too scared to go without t4 altogether. Or that's how it seems right now. I will try splitting my NDT soon...when I have time to rest while it kicks in because the slightest sustained dip in levels and I am straight back into pain, fog, fatigue and vile neuro symptoms.
One of the things that has brought me up short is reading Paul Robbins on topping up NDT with t3 lowers conversion of t4 to t3 because the suppressed tsh tells the liver we don't need more t3 and stores it. (I think I have got the gist of it but link at end). He concurs that a very low dose of NDT with t3 might be OK for some. STTM advise no more, or less than 1.5 grains topped up with t3 or t3 only to clear rt3. I don't think I have rt3 issues at mo...but Paul is basically saying we could create them by mixing t3 with t4.
My last test showed normal t4 and high t3 BUT, unbeknown to me, they took thyroid levels along with per-arranged fasting blood glucose, I had taken my NDT dose the same morning as the draw. I am working on iron levels and cortisol and having those tested.
Um...sorry. my post looks a bit convoluted...got a 1001 questions buzzing in my head.
P.S I note from John Lowe's last interview he used 150 mcg T3 in the morning, which, he said, served him well for over 25 years. I believe but think I'd explode.
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helbell
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Dr. Lowe had his patients dose to 4 grs and if no better or having toxic symptoms from the t4, would switch them to t3, once per day. I wouldn't bother with tests.
I don't understand this suppressed TSH, telling the liver not to convert...makes no sense. Maybe you misread it. Paul's TSH must be suppressed with all the t3 he takes. Dr. Lowe didn't think TSH was an issue, if anything, the TSH test is leaving people untreated.
Do you know what does control the rate of conversion of T4 to T3 in the liver? Or anywhere else?
It is the sort of question which is, in so many ways, absolutely fundamental but I am not sure that we have a good answer. There might well be factors we see having some impact and people have observed various associations. Do we have a full description, properly examined and explained?
Clutter..Why can't she see what she is posting? I reread everything to see if she had vision problems.
I didn't know what "blowed" was either! LOL! We don't use that term here in the states, unless it is of pornographic nature or with bubbles or hair drying LOL!!!
Faith, Helbel posted "Excuse typos...for some reason unknown to me I cannot see the reply box whilst text ing on HU platform. Can be fun and I never said that!"
Hel..i know people can have high rt3 and a high TSH.. Being hypothyroid in itself slows conversion, due to slow bodily processes. ..all organs, lymph system, everything slowed and fluids pooling in tissues and this causing inflammation. And..even if we convert, does it reach the cells? Inflammation puts a stop to that real well.
There is a huge list of things that slow conversion, but i can say that i have not run into an Endo that believes the conversion issue exists unless you have a deficient gene. I was able to get my Endo's to test rt3 levels, even tho they told me they are not useful for determining how to dose. The issue for me, is that whatever keeps me from not converting well, has not been addressed and i don't feel any better by trying to bypass the conversion issue, by using t3 only.
Beats me but here's some of his explanation re my original question.
" This alternative title might be: Why people taking T4 meds feel better for a few days or a week or two when they add T3 but this improvement rarely lasts.
When a thyroid patient beg
ins to add T3 to T4 medication the first thing that happens is that free T3 levels increase. Lo and behold! FT3 levels rise and the thyroid patient feels better. This can last for 3 days, 5 days or even a couple of weeks. It rarely LASTS beyond this. Thyroid patients always expect it to last. Thyroid patients always expect the improvement they feel when they add T3 to their T4 medication to LAST. It is a top up of T3 after all ...... why shouldn't it last?
Well, the reason it never lasts is due to the control system that is in place. The hypothalamus, pituitary, thyroid and liver/kidneys form a control system. This control system is in place to make us feel well ..... but only when our thyroid hormones worked well in the past when we were younger and healthier
Now that our cells need to have far higher levels of free T3 within them for us to feel wonderful and less reverse T3 (because something has changed - see the 'Recovering with T3' book) then we really want this control system to get the hell out of the way and let us take the extra thyroid hormone we need and let it work. Does our control system do that? No it does not!
What happens is that the hypothalamus and pituitary detect more FT3 and demand less thyroid hormone from our own thyroid gland. TSH lowers in response to more T3 hormone in our bloodstream. The liver and kidneys that convert FT4 to FT3 see the lower TSH in the bloodstream and actually decide to operate with a lower conversion rate of FT4 to FT3. Consequently, for those patients who rely on some T4 medication (or some natural thyroid medication or some T4 output from their own thyroid gland) then adding T3 medication can create an initial great result, which is then followed by the control system downgrading this by converting less FT4 to FT3. This results over a few days or weeks in an FT3 level that is just as low as it was to begin with.
That would mean that someone with a damaged pituitary..who doesn't make TSH, could never utilize thyroid hormone and would just die. The rest i understand, but not this.
Thinking about it seems appropriate. Obsessing about it, getting upset by not knowing, and basing changes on these ideas without verification, seem inappropriate.
This particular bit of research fell into my concerns. Ruddy scary enough being torn between being covered by a medic who knows very little or going solo. When an endo tells me to try this, or try that if this does not work then I don't think we are doing anything different and I have to look elsewhere if this or that don't work...if you get my drift. And this isn't a crit of your comment...just creatively rolled off it
Without looking right now, I believe they are hypo because the t3 is being stored as opposed to dispersed in the tissues
. Thyroid gurus say the usual tests apply to see why it is storing and stress or illness will do it as reactive down regulating mechanism .....I think. This says it better stopthethyroidmadness.com/2...
Thanks for all the comments (and the bit of fun). I am decided to try upping dose slightly and splitting. I was really interested to talk to others that use both...maybe they will find it by and by..or I am a complete renegade! I have to say I do like the fast resolution of symptoms from t3 but I am more wary now in the light of Paul Robbins expo, which gives me another area to explore. My crude understanding is he means the body recognizes the additional t3, thinks there is enough and down-regulates conversion of t4 stores, or turns excess into revers t3. I need to read it again plus his links but that's for me to worry about right now xx
I grabbed this info from the front page of the website linked below. If you go to the site you can scroll down this linked page and see more internal links with loads of info. I haven't scanned it thoroughly so can't comment on usefulness but at first glance it seems to cover everything and a bit more.
Quoted text:
"Reverse T3, or rT3 - Understanding The Role This Thyroid Hormone Plays In Hypothyroidism
So, what is reverse T3, and what causes it? There's no quick, simple answer to this question, but let's explore the various layers to this important issue, and how it plays a critical role in hypothyroidism.
Firstly, some degree of rT3 production within our bodies is normal. However, as with every biological system... it’s all about things remaining in balance – or what science calls 'homeostasis'.
Hypothyroidism Is So Much More Than Just A 'Weak Thyroid Gland'
As has already been touched on earlier, one issue that can occur in those presenting with hypothyroidism symptoms is a problem with converting free T4 to free T3.
A range of factors, such as:
• chronic stress (due to severe burns, surgery, prolonged hypothermia, etc.)
• increased free radical exposure
• lack of adequate amounts of dietary antioxidants
• chronic alcohol or other drug abuse
• undue mental or emotional challenges
• excessively low calorie diets or fasts
• liver and kidney disease
• toxic heavy metal exposures
• insulin dependent diabetes
• and even aging itself...
...these can all result in a decreased amount of T4 production from the thyroid gland. This means there is less to convert to the active T3 format of this thyroid hormone.
The Role Of Stress In Creating rT3
Simultaneously, sources of stress - as mentioned above - can create higher levels of cortisol within our bodies, which tends to further inhibit the conversion of T4 to T3.
In fact, aside from inhibiting T4 to T3 conversion, these higher levels of cortisol also have a distorting effect on such conversion, causing the T4 to go into reverse T3 instead... which alas, then competes with normal T3 (triiodothyronine) at the receptor sites.
All these factors add up to there being less of the active form of thyroid hormone, T3, with which to drive out metabolic functions
Again, keep in mind that as a 'mirror molecule' of normal T3, reverse T3 is intrinsically inactive, because it docks onto receptor sites in an upside-down fashion. This in turn prevents proper activation of that receptor site, and only serves to block such sites; it does not activate them.
The more that we are bombarded by a range of constant stressors, so too do we generate ever more amounts of reverse T3, which ends up sabotaging normal metabolic function on a cellular level, causing a drop in basal metabolic rate.
The Role Of Dieting In Creating rT3
Another common factor, especially in the obese populations of the West, is doing too many diets, or being on too restrictive a diet. When the body goes into a fasting mode, it's response is to slow down the metabolic rate in order to conserve whatever little energy intake the body has access to.
Want To Skip Ahead In This 'Reverse T3' Discussion?
The following discourse will obviously flow more logically if you read it as it unfolds below, however, if you're in a hurry and wish to focus on one specific point initially, then simply click on any of the links in the blue box below in order to jump ahead."
We should not forget that as uat we need to have optimal levels of d3 iron magnesium b12 probably more for our bodies to utilise anything. This could be the differences that we find taking medicationa one size fits all.. it doesn't . But this is a very complicated thread for a newbie to get head around ..
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