Thyroid Science
A journal dedicated to truth in thyroid science and thyroid clinical practice

ABOUT US | Home | Journal Staff | Editorials & Latest Postings | Search Engine |
Authors' Guidelines | How to submit Papers | How to Submit Letters |
SECTIONS | Criticism | Case Reports  | Debate | Clinical & Lab Studies | Hypotheses | Letters |

Thyroid Science 1(1):C1-2, 2006

Rejected Letter by
John Dommisse, MD to the Editor of The
Journal of Clinical Endocrinology and Metabolism

Dr. John Dommisse's Website

November 16, 2003

John P. Bilezikian, Editor-in-Chief
The Journal of Clinical Endocrinology & Metabolism
College of Physicians & Surgeons of Columbia University
630 West 168 Street
Mail Box 42
New York, NY 10032, USA
Phone: (212) 305-6886

Re: The "failure" of the substitution of T3 to improve mental
or physical functioning in hypothyroid patients (Oct. 3, 2003)

Dear Dr Bilezikian,

Having treated about 3,500 people with hypothyroidism extremely successfully over the past 14-year period, I am again shocked by the degree to which researchers (1,2) and opinion-makers (3) are still inhibited in their approaches to hypothyroidism treatment by the fear of causing or aggravating osteoporosis or cardiac arrhythmias. Optimizing the serum dialysis free-T4 and -T3 levels in all my patients has not contributed to osteoporosis at all (on the contrary, serial DEXA scans have usually shown dramatic increases in bone density despite my never prescribing any drugs for osteoporosis but using nutritional and metabolic corrective approaches instead); and cardiac arrhythmias are taken care of by making sure there is no functional deficiency of any of the pertinent minerals in the appropriate fluid spaces (RBC/packed cell levels in the case of magnesium and potassium). Not doing these things, and assuming that a "normal" TSH always means normal—even optimal—thyroid hormone function, is causing vast under-diagnosis and under-treatment in millions of patients in the US and around the world. Surveys of patient satisfaction with treatment, and websites devoted to this topic, invariably show deep distrust of the adequacy of their treatment.

The "fatal flaw" in both articles? In adding T3 (in the case of the Western Australia school, in a single daily dose, which is extremely incorrect, and in insufficient amount to even compensate for the loss of T4), both teams still insisted on keeping the TSH within its "normal range," which is not the best approach, in my opinion and that of many others. It is recognized by some that many patients do much better clinically—and don't become osteoporotic or cardiac-arrhythmic, as long as FT4 and FT3 are not above their normal ranges—on thyroid treatment that lowers their TSH level well below its "normal" range. Even the NEJM article in Feb 1999 (4) made the same error but somehow managed to come up with improvement on the substitution of T3 for some of the T4.

So all these researchers are still so hooked into the TSH-only-in-diagnosis/T4-only-in-treatment approach that they can't even envisage adding T3 2-3x/day without subtracting a supposedly-equal amount of T4 in the daily intake. I say "supposedly-equal" because, after the substitution, if the TSH dropped below its "normal range," one or both doses of T4/T3 were then lowered in order to bring the TSH level into its "normal range." So even these published dosages became less when the TSH fell below its "normal" range.

If, as I believe they should, they would go by the accurate (Dialysis) free-T3 and -T4 levels instead, they would find that most people on T4-treatment-only are WAY below optimal in their FT3 level and some would be suboptimal even in their T4 level—in which case T4 needs to be added, as well as T3 being added, to optimize both levels!

One of the biggest losses of function in T3 deficit is life itself, as well as cardiovascular function, due to hyperlipidemia (5,6,7). By optimizing all my patients' T3 (and T4) levels, I have never had to use any statin drug to normalize anyone’s lipid levels. And the only death in my practice in the past nine years was that of a 79-year-old, very obese woman who often could not afford her treatments.

The editorial by Kaplan et al admits that these authors believe that correcting ALL symptoms of ALL hypothyroid patients is an impossible dream. Since they are approaching the subject under the same assumptions as the researchers in the same issue, we can see why!

Yours faithfully,
John V Dommisse MD, FRCP(C)
Member, American Association of Clinical Endocrinologists


1. Walsh JP, Shiels L, Lim EM, Bhagat CI, Ward LC, Stuckey BGA, Dhaliwal SS, Chew GT, Bhagat MC, and Cussons AJ 2003 Combined thyroxine/liothyronine treatment does not improve well-being, quality of life, or cognitive function compared to thyroxine alone: A randomized controlled trial in patients with primary hypothyroidism. J Clin Endocrinol Metab 88:4543-4550

2. Sawka AM, Gerstein HC, Marriott MJ, MacQueen GM, and Joffe RT 2003 Does a combination regimen of thyroxine (T4) and 3,5,3'-triiodothyronine improve depressive symptoms better than T4 alone in patients with hypothyroidism? Results of a double-blind, randomized, controlled trial. J Clin Endocrinol Metab 88:4551-4555

3. Kaplan MM, Sarne DH, and Schneider AB 2003 Editorial: In search of the impossible dream? Thyroid hormone replacement therapy that treats all symptoms in all hypothyroid patients. J Clin Endocrinol Metab 88:4540-4542

4. Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ 1999 Effects of thyroxine as compared with thyroxine plus triiodothyronine in patients with hypothyroidism. New Eng J Med 340:424-9

5. Dullaart RP, vanDoormaal JJ, Hoogenberg K, Sluiter WJ 1995 T3 rapidly lowers plasma lipoprotein-a, apo-b and LDL-cholesterol in hypothyroid subjects. Neth J Med 46,Apr:179-84

6. Fowler PBS, Stubbs P 1992 Asymptomatic hypothyroidism and hypercholesterolemia. J Royal Soc Med 85,April:244-5

7. LeMar HJ, West SG, Garrett CR, et al. 1991 Covert hypothyroidism presenting as a cardiovascular event. Am J Med 91:549-52


© 2008 Thyroid Science