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!