Discussions that mention thyroxine

General Health board

Quote from typhoidmary:
That is your opinion - you have no need to be so dogmatic since my source is very definetely up to date (Royal College of Physicians). T3 causes arrhythmias unlike T4 which is converted peripherally to T3 and avoids cardiac problems.

Too much T4 can cause cardiac problems. I said:

Quote from Gopherhead:
Correct dosage of T3 does not cause cardiac problems.

It is not my opinion, it is, however, the opinion of many endocrinologists in the field:

Danzi S, Klein I. Thyroid hormone and the cardiovascular system. NYU School of Medicine and North Shore LIJ Research Institute, Manhasset, NY, USA. Minerva Endocrinol. 2004 Sep;29(3):139-50.

Agid O, Lerer B. Algorithm-based treatment of major depression in an outpatient clinic: clinical correlates of response to a specific serotonin reuptake inhibitor and to triiodothyronine augmentation. Int J Neuropsychopharmacol 2003 Mar;6(1):41-49.

Bunevicius R, Jakubonien N, Jurkevicius R, Cernicat J, Lasas L, Prange AJ Jr. Thyroxine vs thyroxine plus triiodothyronine in treatment of hypothyroidism after ********ctomy for Graves' disease. Endocrine 2002 Jul;18(2):129-33.

Woeber KA. Levothyroxine therapy and serum free thyroxine and free triiodothyronine concentrations. J Endocrinol Invest 2002 Feb;25(2):106-9.
Quote from typhoidmary:
A quick browse of websites shows "Liothyronine sodium is contraindicated in patients with cardiovascular disorders or angina of effort"; Dr Wartofsky said of liothyronine "we are making patients mildly thyrotoxic for a while and they feel better. But over a long period of time there are adverse effects on bone and the heart."

A quick look at some more recent literature :

The following is an excerpt of a paper written by Dr. Barry Durrant-Peatfield. It also touches upon heart effects of T4 and/or T3 treatment. If you want the entire contents of the excerpt, look up the doctor's name using the Board's Advanced Search:

"The net result very much too often in clinical practice is to under-dose. To provide full remission of symptoms, the level in the tissues of thyroid hormone should be as high as possible, short of too much. (The patient/doctor monitoring to achieve this is described later). The situation is worsened by a tightly held misapprehension in many quarters that there are grave risks associated with overdose. These are largely apocryphal and must be corrected. Probably most widely held, is that thyroid overdose is bad for the heart. The risk is there if coronary artery insufficiency, previous M.l or incipient failure already compromises the heart; the risk of over working a damaged heart is obviously undesirable. The healthy heart will not be damaged by minor degrees of overdose, whether by accident or design; and is rarely much affected even by high levels of thyroid hormone, as in Grave’s Disease.

Another anxiety is osteoporosis. There is a risk in sustained overdose, and untreated hypothyroidism, but this is still not certain. There is NO risk of osteoporosis in thyroid supplementation in correct, physiological doses obviously; and in any inadvertent minor overdose is rapidly detected by monitoring, and therefore of no consequence either."

Excerpt from an interview with Dr. John V. Dommisse on the effects of T4/T3 treatment, in particular, on bones:

The danger of osteoporosis is way-overblown and is the reason why many hypothyroid cases are not diagnosed as such (because then the physician has to subject himself to this supposed high risk of being sued for having caused or aggravated the osteoporosis). It is strange that the free-T3 level should be picked on in this fearful strategy because hardly any of the studies that have been done on thyroid treatment causing osteoporosis have even measured the free-T3 levels of those patients! In fact, the free-T3 level is seldom obtained, period. And this is the level that does 90% of the thyroid function! The main reason why I know the fear of osteoporosis is overblown is that all my patients who are both hypothyroid and osteoporotic see their bone mineral density x-ray scans not only not deteriorate every year, but actually improve - by as much as 30 percentage-points in one year! If osteoporosis can be caused or aggravated by aggressive, hi-normal thyroid treatment, then surely my patients would be prime suspects to show this phenomenon. But they don't. Admittedly, I do also correct many mineral, vitamin, amino-acid and other hormone deficiencies, many of which cause or aggravate osteoporosis, but at least I have proven that, in a fairly-unique practice that does attend to such deficiencies, there is not only no danger of osteoporosis, there is reversal of osteoporosis. And this is without the use of Fosamax, calcitonin or any other drugs that are usually prescribed for osteoporosis."

Excerpt from a paper by Dr. Dommisse that you can also find in the Board's archived posts listing the ten most common thyroid myths. This is Thyroid Myth #9 and the author's comments on it:

"(9) "Keeping both the FT4 and FT3 levels at the high ends of their normal ranges will cause osteoporosis": This concern was merited 30-50 years ago, when much-higher doses of thyroid hormone were used in the treatment of most cases of hypothyroidism. One of us (JVD) has not observed this complication in over eleven years of this more-aggressive treatment (unpublished data). In fact, his treatment_optimized hypothyroid osteoporotic patients' bone density scans not only don't deteriorate from one year to the next but almost-invariably improve, without the use of elindronate, calcitonin or any other drugs. This means that, for there to be 'overtreatment' of hypothyroidism, it has to be more substantial than is currently thought. Concurrent correction of other factors, such as deficiencies of vitamins, minerals, other hormones, and amino-acids, seems to maintain and extend bone density, even in the presence of optimal or 'aggressive' treatment of hypothyroidism."

Four studies and their references showing no ill-effect on bones ~
Study #1 ~ Journal of Gynecological Endocrinology
Gynecol Endocrinol 1998 Oct;12S(5):333-7, "Bone mineral density in premenopausal women receiving levothyroxine suppressive therapy."

Study #2 ~ Journal of Clinical Endocrinology and Metabolism
J Clin Endocrinol Metab 1994 Apr;78(4):818-23, "Carefully monitored levothyroxine suppressive therapy is not associated with bone loss in premenopausal women."

Study #3 ~ Thyroid
Thyroid, 1995 Feb;5(1):13-7, "Suppressive doses of thyroxine do not accelerate age-related bone loss in late postmenopausal women."

Study #4 ~ Journal of Hormonal and Metabolic Research
Horm Metab Res 1995 Nov;27(11):503-7, "A slightly suppressive dose of L-thyroxine does not affect bone turnover and bone mineral density in pre- and postmenopausal women with nontoxic goitre."

This statement is from Dr. John Lowe, noted expert on fibromyalgia, CFS, osteoP, and hypoT:

" In the 1970s and 1980s, many faulty studies were published that led to the erroneous conclusion that TSH-suppressive dosages of thyroid hormone decrease bone mineral density in most patients. Some conventional endocrinologists wrongly extrapolated from these studies that TSH-suppressive dosages lead to osteoporosis and increased risk of bone fracture. Better designed studies have shown that these conclusions were wrong, and the only group of patients really at risk for substantial loss of bone density from the use of TSH-suppressive dosages are post-menopausal women who previously had Graves’ disease."

The Earth used to be flat. The Earth used to be the centre of the Universe. Things change.