The article is too full of medical-speak for me to understand. But I understand these two concluding sentences.
"In conclusion, euthyroidism is not restored in plasma and all tissues of thyroidectomized rats on T4 alone. These results may well be pertinent to patients on T4 replacement therapy."
Because it has been decreed that levothyroxine is the 'perfect' replacement, regardless of what the patient says/feels on it.
If you refer to the BTA guidelines, it's there in black and white. They have also made False Statements re natural dessicated thyroid hormones to try to warrant their statements.
It seems frighteningly like a conspiracy around the world between Big Pharma and the medical profession. I have had TT and absolutely know that T4 alone caused me all kinds of large and small ailments. Am now on the T4/3 combo, which makes a huge difference, although still not perfect. Neither is NDT good for me. The answer is to do more to save thyroids and not regard removal as just as unfortunate little incident, successfully treated by a little white pill.
Shocking and very sad - to think that this has been known from 1995. Why are doctors in this field so willing to go along with what is happening? So few speak out - and look what happens to them - I wonder what the others secretly think. Are they all brainwashed or do sympathetic young doctors see what is happening and avoid that area of medicine? endocrinology seems to be a field of medicine where so many of the patients are thought to be hypochondriacs - or that's how it seems to me.
Interesting and I can understand the comments and frustration but unfortunately life isn't that simple! It's a long way between getting from a rat to a human being. Had I tecognized any of the names either on the research team or the previous work done by others I would have asked questions. Usually as a scientist in this sort of field you have to get some medics on board and even they cannot do on humans what may have been done to these rats. Even when one gets through this barrier there are years of trials. It was a fair time ago but it may have been disproved, not saying it was, further down the line or further testing not conclusive.
I can tell you of one scenario my late husband was involved in that got no further when he was involved in a serious RTA but he wanted to obtain some cord blood. Why I have no idea but probably something to do with stem cells, I'm going back over twenty years. I don't think he would have much problems in obtaining this my getting medics on board and I'm sure a newly delivered mother wouldn't really be concerned about the bit usually disposed of but would she be willing to have her beautiful new baby kept under sevailance for numerous years-probably not and that's before you look at the practicalities of keeping in touch. Don't want to put a damper on anything that looks promising. Just wanted to point out it doesn't mean it will come to fruition and if it does it will take literally years.
There's also a follow up by the same team, showing that combined T4/T3 treatment does produce normal results in all tissues of a thyroidectomised rat. I'd love to read the full paper but I can't find it for free anywhere.
So hears something from "the past", used on real people. Seems to be neglected today as there's preference for calcium channel blockers, angiotensin 2 blockers and of course statins, another blocker, rather that using T3!
Love to know if someone knows of validation or repudiation of this paper.
Neth J Med. 1995 Apr;46(4):179-84.
Triiodothyronine rapidly lowers plasma lipoprotein (a) in hypothyroid subjects.
Dullaart RP1, van Doormaal JJ, Hoogenberg K, Sluiter WJ.
Author information
Abstract
BACKGROUND:
Increases in plasma low-density-lipoprotein (LDL) cholesterol and apolipoprotein B (apo-B) are well known in primary hypothyroidism, but it is uncertain whether thyroid dysfunction is associated with elevated levels of the atherogenic lipoprotein (a) (Lp(a)).
METHODS:
The effect of short-term hypothyroidism on plasma Lp(a) was studied in 14 patients who had undergone a total thyroidectomy because of a well-differentiated thyroid carcinoma. They were studied 2 weeks after withdrawal of triiodothyronine (T3) therapy and 7 (5-9) weeks after resumption of T3 treatment (75-100 micrograms T3 daily). Fourteen euthyroid subjects served as controls.
RESULTS:
In the hypothyroid phase the athyreotic patients had higher levels of Lp(a) (105 [12-536] vs. 42 [1-321] mg/l, p < 0.05), apo-B (p < 0.001) and LDL cholesterol (p < 0.001) as compared with the euthyroid control subjects. T3 therapy lowered Lp(a) by 29% to 50 (12-535) mg/l, p < 0.01. Apo B and LDL cholesterol fell by 42% (p < 0.001) and by 53% (p < 0.001), respectively. After resumption of T3 therapy the levels of Lp(a), apo-B and LDL cholesterol were not different from those of the control subjects. The mean percentual decreases in Lp(a) and in apo-B were similar, although the individual changes in Lp(a) were more variable.
CONCLUSIONS:
Short-term hypothyroidism increases plasma Lp(a) and T3 therapy rapidly lowers Lp(a) together with apo-B and LDL cholesterol. Our findings support the hypothesis that thyroid hormone regulates plasma Lp(a) and apo-B in a parallel manner. Elevated concentrations of Lp(a) in combination with LDL cholesterol may be involved in the increased risk of cardiovascular disease assumed to be associated with hypothyroidism.
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