My new GP (about last august) let me try levo, and has allowed me to make my own decisions as to increases. I always say what I am thinking and ask her if o.k. I am a lot better than I was but still a lot of symptoms. As I have RA I don't know what is causing what.
A couple of weeks ago I had a T3 test. 3.6 (3.5-6) TSH suppressed T4 at top.
I am wondering should I try for higher levo, or, I may be pushing it, to ask for T3 to be included.
Spoke to local pharamacist (shop opened 2 yrs ago) and he said not had a T3 script in that time.
I don't want to rock the boat some opinions please.
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siskin
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Siskin, I don't see why you should be shy or tactful about requesting T3. Suppressed TSH + high FT4 + low FT3 = poor T4 to T3 conversion. Tell your GP that you think you are still symptomatic because of your low T3 and you think Liothyronine (T3) might be helpful, but be advised that some CCGs have instructed GPs not to prescribe T3 without an endo recommendation.
Thank you for that Clutter, I hope CCG have not put that in place as there is not a sympathetic or should I say enlightened endo in my area. Diabetes endos by the dozen, but none put down thyroid disorders as specialist subject. Several are gender re-asignment and other rarer disorder specialist.
I fought for nearly 4 yrs. with the help of this forum, to get this far, I don't want to blow it now.
The fact that pharmacist hasn't seen a scrip in last 2 yrs was concerning me. They are only a small independent shop.
Siskin, If you don't make the request you certainly won't get T3. If GP says no, you'll either have to go the endo route and hope you get someone helpful or you'll have to think about self medicating.
If your fT4 is top and TSH is suppressed, you could realistically reduce T4 to 75 mcg and take 5 mcg T3. (thyroxine, liothyronine.... let's get the correct words in here....;0) That may get your TSH a bit less suppressed, keep everyone sort of happy and increase the fT3. That would put you at 85 mcg T4 equivalent but since it works differently, it may be alright. What's 5mcg T3 between friends? Nothing much. If it's not enough raise to 10 mcg: 5 mcg twice a day but go slow. T3 gives a bit of a jolt initially. \
Just watch out for hyper symptoms like global anxiety and boomboom heart beats.
5 mcgs of T3 wont stimulate any receptor sites. I was told by Dr Lowe that these amounts are not enough for a gnat. If the T4 isn't converting then the T3 receptor sites on the cells need stimulating and this small amount will not do that.
Hi that all depends on how low you are. I take 100 mcgs T4 and 37.5 mcgs of T3. My doctor here is not happy and won't prescribe for me, even though I have no thyroid tissue at all, but I am well on this. I go to Dr Hertoghes clinic and the doctor I see there said I have no signs of over-stimulation even though my TSH is very suppressed. A suppressed TSH doesn't mean you are hyper as the TSH is measuring the signal from the pituitary to the thyroid gland, it's a message and has no correlation to how much T3 is present in the T3 receptor sites on the cells.
I would just say to your doctor can you please just try some T3 to add to your T4. The tablets on the NHS I think are 20 mcgs but I can't say how much to take, it's up to how you feel.
It really is trial and error with thyroid treatment, what suits one may not suit another. Some do well on T4, T3 combination and some on NDT and some T3 only. Your body will tell you what's right. Good luck
My blood sugar responses tell me what my limit is. When i was taking 100 mcg T4 and 12.5 mcg T3 i had a delayed insulin response and for the first hour after eating anything with carbs, sugars would rocket to over 15. Once to 19. Then rocket down to 3.2. I'm not diabetic though. With 125 mcg T4 and 6.25 mcg T3 blood sugars are normal. I'll find out next week what the fT3 is at this dose. It was 'ideal' 'prefect'.... um, well, it didn't feel perfect and blood sugar was alarming. The higher the T3 dose, the more my ears were ringing. At current dose, they are not. So maybe I'm a gnat.
Lol no your not a gnat. Have you tried reducing the T4 and taking that amount of T3, perhaps that will work. It's normally too much T4 that makes the ears ring, well that's what I have found in the past.
Oh yes. 88 mcg T4 plus 18.75 mcg T3 = ear ringing. And blood sugar problem. To find out if it was T3 at fault, I took 25 mcg one day. Not ever trying that again. Really bad. On 88/10 I was hypo, ears were not ringing but I puffed up like a soufflet.
I'll see what the blood levels on Monday. Regardless, either I go up to 150 mcg T4 or stay where I am.
What a game this is. When we are young and our hormones are balanced we just accept it but as we grow old and the hormones fall away to get them balanced is a nightmare. I had my gland removed (lingual) at age 42, guided by T4 and the bloods fell into a near coma for 14 months, fibromyalgia, ME, CFS you name it I had it, couldn't walk properly, could only drink water at one time, allergic to everything. It was Dr Peatfield that saved me, 20 mcgs T3 and it was as though a light switched on. I then went to USA as I still had fibro but could walk again then they advised taking the T3 right up, ultra sound and exercise to tolerance, which I did and it got rid of the fibro. As the years have gone on I am better with some T4 and T3, however, I am on cortisol which is helping with the conversion, without it I couldn't convert the T4 properly. T3 only now isn't enough so it shows how the body changes. Good luck with your balancing, only you know what you need.
Have you checked your adrenals by a saliva test? Genova do the test.
I've been hypo since my teens. Been on thyroxine since 1982. Only felt good while on 150 mcg. That was with physician who treated symptoms. Since then it's the god of TSH. Unfortunately if my TSH goes to 1.0 my fT4 and fT3 are hypo. Odd too that the actual gland is normal size and no weird things in it. You'd think after taking replacement for so long it would atrophy or something. It's just sitting there doing nothing. I don't like T3. But seems I'm stuck with it.
Not many physicians that treat symptoms these days, the blood tests rule. My TSH is 0.01 and I feel fine. So if when your TSH goes to 1 you feel bad then keep it more suppressed. Have you ever had glandular fever? Just out of interest, if you have it does damage the thyroid tissue, not many doctors know this. Well no if your gland is working and you are suppressing it then as soon as you come off the meds it will or should start working again but it won't give you what you need if it's damaged or not 100% right.
I love T3, I would be bedridden without it. I do wonder if your adrenals are not working properly as the active T3 would stress your adrenals and although you would automatically blame it on the T3 it maybe you need the T3 but your adrenals aren't strong enough to take it.
I would ask for T3 as you my not be converting sufficient T4. If you privately mail me I can give you Dr Tofts conference notes which states some people are good on T4 and T3 some T3 and some Ndt. Lynthip@aol.com
Just back off hols and reading up my emails. My lovely GP has just retired and new one has never heard of Cytomel!. My old GP prescribed 40 mcg per day which saved my life. New guy is taken aback and causing trouble. Please can you pm the Toft details just in case .
I am attaching it anyway, in case you would like to research PubMed and Google to see if you can find anything. If you can't, PM me your e mail address, I am happy to send you a copy of the article even though the link doesn't seem to work any more.
"The inflammatory cytokines IL-1, Il-6, C-reactive protein (CRP), and TNF-alpha will significantly decrease D1 activity and reduce tissue T3 levels (105-113). Any person with an inflammatory condition — including physical or emotional stress (243-248), obesity (248-252), diabetes (248,249,253), depression (254-257), menopause (surgical or natural) (258), heart disease (248,259,260), autoimmune disease (lupus, Hashimoto’s, multiple sclerosis, arthritis, etc) (114,115,164,265), injury (266), chronic infection (261,262) or cancer (267-269) — will have a decreased T4 to T3 conversion in the body and a relative tissue hypothyroidism. The inflammatory cytokines will, however, increase the activity of D2 and suppress the TSH despite reduced peripheral T3 levels; again, making a normal TSH an unreliable indicator of normal tissue thyroid levels (105-113)
There is a direct inverse correlation between CRP and reduced tissue T3 (112,270), so individuals with elevated CRP (greater than 3 mg/l) or other inflammatory cytokines will have a significant reduction in cellular T3 levels. The suppression of intracellular T3 levels correlates with the degree of elevation of CRP, despite serum thyroid tests being “normal” (112,270). Thus, if any inflammation is present, which is found in numerous clinical and subclinical conditions (as above), the body will have lower cellular T3 levels that are often inadequate for optimal functioning; but the pituitary will have increased levels of T3, resulting in a lowering of the TSH that would potentially be inappropriately interpreted as an indication of “normal” thyroid levels.
Thus, any person with an inflammatory condition will have diminished tissue levels of T3 potentially severe enough to cause symptoms, but these symptoms will not be detected by standard thyroid testing. Additionally, due to the reduced T4 to T3 conversion induced by the inflammation in these conditions, effective treatment must include T3 (combination or, ideally, timed-released T3). Also, due to the inflammatory suppression of TSH, not only is a normal TSH necessarily an indication of euthyroidism (normal thyroid), but also a suppressed TSH is not necessarily an indication of excessive thyroid with treatment. Rather, free T3 and reverse T3 levels along with clinical parameters should be used to determine optimal replacement doses of thyroid.
Additionally, inflammation will stimulate D3, producing more reverse T3, further causing cellular hypothyroidism not detected by TSH testing by suppressing intracellular T4 to T3 conversion and blocking the T3 receptor inside the cell (271)."
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