Quotes of Interest
1. Low thyroid is associated with an increased risk of coronary artery disease, heart attack, heart enlargement, stroke, infections, and cancer. Coronary-Artery Disease in hypothyroidism. The Lancet
2. Many physicians have realized that patients can be profoundly hypothyroid and still have normal values of TSH and Free T4. In a recent issue of the British Medical Journal(1) several physicians noted this by stating, We wish to question present medical practice, which considers abnormal serum concentrations of free thyroxine and thyroid stimulation hormone-those outside the 95% reference interval-to indicate hypothyroidism but incorrectly considers normal free thyroxin and thyroid stimulation hormone concentrations to negate this diagnosis. It is unusual for doctors to start thyroxin replacement in clinically hypothyroid but biochemical euthyroid patients. They note that of 80 patients who were diagnosed as hypothyroid on established clinical (signs and symptoms), only 5 patients had abnormally low T4 levels and only 4 had abnormal high TSH levels. The averaged TSH concentration was below the middle of the reverence range. They stat that these people deserve treatment other wise they are condemn to many years of hypothyroidism with its complications and poor quality of life. British Medical Journal, 1997.
3. For over 80 years, before the advent of TSH testing, physicians with outstanding ability have regularly treated thyroid patients with enough thyroid to clinically normalize their patients regardless of dose. The maxim of the day before TSH arrived was to give enough thyroid until the patient felt better. Medical student are still repeatedly told to treat the patient and not the lab values, but this quickly gets forgotten and disregarded when it comes to thyroid. The 80 years of experience with thyroid hormone treatment demonstrated that people would normally need 200-400 micrograms of T4, such as Synthroid, or 3 to 5 grains of desiccated thyroid. The long-term studies of over 40 years show no side effects from such doses and thyroid is probably the safest long-term drug of the Century. When TSH testing came into use in 1973, the average doses dropped to 1/3 of the doses previously used.(2) British Medical Journal, 1999.
4. In a study in the 1997 Journal of Endocrinology and Metabolism, clinical signs were compared to blood tests. The authors demonstrated that individuals have varying degrees of thyroid resistance in different tissues. The authors describe this as a metabolic hypothyroidism in different tissues. They state tissue hypothyroidism at the peripheral target organs must be different in the individual patient. The authors summarize their findings by stating that they agree with the statement in a endocrinology text book stating, The ultimate test of whether a patient is experiencing the effects of too much or to little thyroid hormone is not the measurement of hormone concentration in the blood but the effect of thyroid hormones on the peripheral tissues”. The Journal of Clinical Endocrinology & Metabolism 1997 Basic and clinical endocrinology, 3rd ed. London: Appleton.
5. Thyroid and weight loss-1997 study It was shown that T4 preparations such a Levoxyl and Synthroid resulted in very minimal increase in metabolism while supplementation with T3 was shown to increase metabolism by an average of 18%. For a person consuming a 2000 calorie diet, 18% is equivalent to burning an extra 360 calories per day. Thus giving T3 would equate to approximately a 40 pound weight loss in a year. This is equivalent to approximately jogging on a treadmill for 1 hour per day. If we would simply optimize everyones thyroid, we would not longer have the obesity crises in this country. This could easily be remedied and drastically cut he incidence of diabetes, heart disease, hypertension, stroke and cancer. Thyroid should never be given as a weight loss medication but appropriate replacement with the proper preparations often elevates a number of symptoms, often including continued weight gain. The Journal of Clinical Endocrinology & Metabolism, 1997.
6. Reverse T3 blocks T3 action and lowers metabolism Res Exp Med 1997.
7. It is extraordinary that more than 100 years since the first description of the treatment of hypothyroidism and the current availability of refined diagnostic tests, debate is continuing about its diagnosis and management. Anthony Toft and Geoffrey Beckett BMJ 2003 (8 February); 326:295-296
8. Thyroid and regaining lost weight after dieting T3 falls during acute and chronic calorie restriction (dieting) and reverse T3 increases during acute and chronic calorie restriction, blocking thyroid effect and lowering metabolism. Is this a factor why lost weight is usually regained? Am J Clin Nutr, 2000.
9. Thyroid hormones improve blood flow to heart and prevent heart attacks. Thyroid, 1998.
10. There is an increased risk of arrhythmias if your T3 levels is low and/or your reverse T3 levels are high. This is opposite of what most doctors think. Journal of Cardiology, 1993.
11. Thyroid stimulating hormone concentrations above 2 mU/l are associated with an increased risk of hypothyroidism.. subclinical hypothyroidism is common, especially in elderly women ..the presence of subclinical hypothyroidism or thyroid antibodies increases the risk of developing overt hypothyroidism and the risk is even greater (about 5% a year) if both are present together. thyroid stimulating hormone concentrations above 2 mU/l are associated with an increased risk of hypothyroidism.case finding, especially in women over 40 with non-specific symptoms, is currently the best approach to detect previously unsuspected hypothyroidism. modest symptomatic benefits occur with thyroxine treatment in some patients with subclinical hypothyroidism, and lipid profiles may also improve .monitored thyroxine treatment, maintaining normal thyroid stimulating hormone concentrations, has no adverse effects. A P Weetman, Professor of Medicine.
12. “. . . even within the reference range of around 0.5-4.5 mU/l, a high thyroid stimulating hormone concentration (>2 mU/l) was associated with an increased risk of future hypothyroidism. The simplest explanation is that thyroid disease is so common that many people predisposed to thyroid failure are included in a laboratory’s reference population, which raises the question whether thyroxine replacement is adequate in patients with thyroid stimulating hormone levels above 2 mU/l.” A P Weetman, professor of medicine (British Medical Journal,19th April 1997.
13. “Why are we following a test which has no correlation with clinical presentation? The thyroidologists by consensus have decided that this test is the most useful for following treatment when in fact it is unrelated to how the patient feels. The consequences of this have been horrendous. Six years after their consensus decision Chronic fatigue and Fibromyalgia appeared. These are both hypothyroid conditions. But because their TSH was normal they have not been treated. The TSH needs to be scrapped and medical students taught again how to clinically recognize low thyroid conditions.” David Derry M.D., Ph.D.
14. “A typical (statistical) reference range for thyroid-stimulating hormone (TSH) in many laboratories is around 0.2-5.5 mU/L. However, the 20-year longitudinal Whickham survey indicated that individuals with TSH values greater than 2.0 mU/L have an increased risk of developing overt hypothyroidism over the next 20 years. Drs Colin M Dayan, Ponnusamy Saravanan, & Graham Bayly, Whose normal thyroid function is better yours or mine? The Lancet, 3 Aug 2002; 360(9330): 353.
15. BMJ 2003;326:1087 (17 May), doi:10.1136/bmj.326.7398.1087 . . . We have long taken the view that most hypothyroid patients are content with a dose of thyroxine that restores serum concentrations of thyroid stimulating hormone to the low normal range. However, some achieve a sense of wellbeing only when serum thyroid stimulating hormone is suppressed, when we take care to ensure that serum tri-iodothyronine is unequivocally normal.
Until valid evidence shows that such a policy is detrimental we will continue to treat patients holistically rather than insist on adherence to a biochemical definition of adequacy of thyroxine replacement. The issue of whether a little too much thyroxine is dangerous is likely to evaporate when appropriate preparations become available to allow treatment of hypothyroidism with both tri-iodothyronine and thyroxine. . .A D Toft, consultant physician, Endocrine Department Royal Infirmary of Edinburgh, Edinburgh EH3 9YW
16. Dr. Dommisse to the JOURNAL OF CLINICAL ENDOCRINOLOGY submitted the following Letter to the Editor on the 16 th November 2003and it was rejected. It was in response to an article stating that adding T3 to treatment was a failure.
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 degree to which researchers 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, 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!
John V Dommisse MD, FRCP(C)
Member, American Association of Clinical Endocrinologists
17. Many years ago, while I was in medical school, physicians were taught to diagnose hypothyroidism, or low thyroid function, by using the newly discovered method of measuring the metabolic rate while the patient ran on a treadmill. Doctors thought this was a new test and that they finally had a way to identify patients with underactive thyroids. Doctors congratulated themselves on being so clever. But then a new test came out. The new test measured protein-bound iodide (PBI). When doctors began using the PBI test, they realized, `Oh, w missed diagnosing so many people with a low thyroid, but this new test will now pick up everybody who has a problem. The doctors patted themselves on the back and told all their newly discovered thyroid patients that it turned out that they were not crazy they just had a low thyroid. The doctors were comfortable that they could now determine with certainty when someone had a thyroid problem.
Then the T4-level thyroid test was developed and the doctors said, `Oh, that silly old PBI test. It missed so many people with a low thyroid, but this new test will find everyone. Then the T7-level test came out, and then the thyroid-stimulating hormone (TSH) test. Modern medicine is now into the fourth generation of TSH tests, and with each new test, doctors realized they missed many people with under active thyroids. You would think that we doctors would finally catch on. My impression, and the impression of many other physicians is that the current method of testing still misses many people with underactive thyroids. Therefore, doctors must treat the patient, not the blood test. From Fatigue to Fantastic Hormones The Bodys Master Control System.