Hi I am on T3 only and my TSH is 4.7. I have been told by Doc that this is right but I feel dreadful. The FT3 is 5.9 and I am on 45mcg split during day. Any help would be great. Thanks Linda
TSH on T3 only: Hi I am on T3 only and my TSH is... - Thyroid UK
TSH on T3 only
I would expect TSH to be suppressed when on a medication containing T3 (mine is <0.02), but unfortunately most doctors don't seem to be aware of this I think you need an increase. Xx
Dr S told me that any T3 containing medication will supress the TSH (mine is 0.03) and even the endo agreed with that.
Yes my endo knew this but not any of the GPs I've seen at my practice
Perhaps I might start to feel better on more T3. My TSH has been all over the place, mostly very high. My SST test was 400 but they do not think I need adrenal support. Thanks Linda
I think you definitely need an increase of T3 to bring your TSH down.
The difference between the lifetime of T3 and T4 in the tissues is considerable. If you take in a T3 tablet say once a day, then after 24 hours, half that T3 will have gone. On the other hand, if you take in an equivalent T4 tablet, then it takes 7 days for half that T4 to be used up. Some of the problem with T3 only is that, taking daily tablets, your FT3 will bounce up and down in levels significantly over 24 hours, much more than happens with T4 (only about an 8% change of T4 in 24 hours and even less for the T3 produced from the T4). Summarizing, taking T4 only doesn't subject your body to such big fluctuations in hormones over the day as T3-only will. This T3 "bounce" may not be good for your feeling of health.
These are two extracts from Dr Lowe's archived site re T3 and on T3 in general.
Dr. Lowe: The short time that T3 is in the circulating blood isn’t the limit of its beneficial effects on the body. When T3 binds to T3-receptors on genes, the binding regulates the transcription of mRNAs, and the mRNAs are later translated into proteins. The transcription and translation initiated by the binding of T3 to T3-receptors occur in waves, and these waves far outlast the T3 that started them at the chromosomes. Moreover, the newly synthesized proteins themselves far outlast the transcription and translation. As a result, a single dose of T3 will be long gone from the patient's system before he or she experiences most of the benefits of that dose—a molecular and metabolic yield that may smoothly spread out over one to three days. The "rocky road" ( August 7, 2001
and
You asked, if we don't have T4 receptors, "then why do we need T4 supplementation rather than just T3 alone?" With rare exception, we don't.
No one can rationally defend T4 supplementation on scientific grounds. I say this because the widespread use of T4 supplementation is not based on scientific studies that show it to be safer or more effective than the use of T3 alone. Instead, its widespread use is the result of a financial venture between the endocrinology specialty and corporations that profit from sales of the most commonly prescribed brands of T4.
web.archive.org/web/2010122...
Sorry to disagree somewhat with Dr Lowe's interpretations. For that's all they are, note the word "may" - no scientific proof that I know shows that the body response to periodic T3 only dosage is completely "smoothed out" in the way he envisages. In normality the body produces T3 steadily from both the thyroid and T4-T3 conversion in the cells. There is no diurnal fluctuation in T3 levels, except maybe temporarily in severe systemic illness, where the balance between T3 and rT3 can change as the underlying illness changes. Any "bolus" of T3 will have a "wavelike" up and down effect (stimulus followed by lack) on the results of T3 action, however much it may be partially smoothed out by delayed effects of protein synthesis etc. T3 alone can be dangerous especially in people with a tendency to heart problems - arrhythmia etc., and especially in the elderly. It's also difficult to control as a daily dose to mimic proper thyroid output because of the combination of its short lifetime and vigorous hormonal activity. The best way forward in my opinion is to combine T4 and T3 in slow release format so as to mimic the body's natural production of both hormones, both in steadiness and in relative and absolute amounts. T3-alone, I don't like as a general treatment. It's better to let at least some of the T3 be produced from T4, as occurs naturally, because this is a process that responds automatically to demand, producing the active hormone T3 from the prehormone T4 as the body requires it..
Diogenes, just to clarify, you don't believe that TSH and T3 have a circadian rhythm as shown by Russell et al?
jcem.endojournals.org/conte...
And you don't believe that some patients seem to do better on T3 alone? Just curious. PR
I firmly believe in the circadian rhythm for TSH. This is wellknown. However, looking at Russell et al's data, its striking a) that subjects differed very much as to the strength of the FT3 rhythm and b) how relatively puny the effect (real as it is) actually showed itself. The most affected person wrt FT3 showed about a 12% change top to bottom of the response curve. Another person had virtually no response change. The average was about 8%. Taken as difference from the mean, the change was +/- 4%. Given the CV% for any FT3 assay measurement as at best a 3% inaccuracy, then the effect is very close to the sensitivity of the assay itself at that point. Contrast that with the TSH curve, whose percent difference top to bottom was close to 60%! From the mean that's +/-30% difference. So, yes there is a FT3 circadian rhythm but it's marginal and compared with the TSH change, negligible. So, this doesn't change my opinion that FT3 is pretty constant as regards measurement accuracy over the day.
Regarding T3 only as a supplement. Evolution has repeatedly come up with a strategy that ensures that all tissues in a body receive the hormonal doses uniquely appropriate for their needs. This strategy is to produce an inactive prohormone (like T4) that circulates throughout the body and is then locally converted to the active hormone where it is needed and in the quantity it is needed. This is true of eg T4, insulin, and the vitamin (really a prohormone) vitamin D.
Therefore to offer direct a given dose of T3 to a patient who is hypothyroid may be OK for some tissues, inadequate for others and too much for yet more. Only the moderating influence of T4 will help to give all tissues the doses they need through their appropriate conversion of T4 to T3 actually in the local position. This is partly why I don't like T3-only regimens. But also I don't like it because of the short half life of T3 and its vigorous hormonal activity. And I don't like natural thyroid extract either, because the T3 content isn't properly controlled. We do not know how T3-only would affect a patient in the long term therefore. Both the strategies are in my eyes as deficient in their own way as the T4-only strategy. As a plea for closer relationships with nature, I think that T4/T3 slow release combination would mimic as closely as possible the natural state of affairs in health. But I fear it won't come about, because of the "she'll do!" attitude in medicine - ie if you can get away with it you do it even if it's not optimal. And perceived expense of course. The majority of hypothyroid people get on OK with T4 only, so long as they ignore the "normalise TSH" dogma. The minority don't, and it's these who need alternative strategies.
Out of interest, when did you take your last T3 before your blood test? Mine was in the morning so I didn't take any T3 after the early evening before it. Then my TSH was 5.9 and my GP was happyish. He said it was a little over what it should be but not high enough to worry about so he thought I was on the right track with my T3 dosage. I knew I was nowhere near right but didn't argue because I'm going it alone and hadn't asked for the TSH test anyway. I do wonder what I should be aiming at though and how to achieve a meaningful test in terms of checking that my dosage is ok.