|
|||||||
|
|
 |
||||||
|
This approach is now explained much more fully in my new copyrighted paper that is for sale, as Natural Medicine Letter Vol. 4, No. 2 (March 2000), for $10, on the Order page at the end of this website. However, a brief summary of this approach is available here. This summary was published in the July 1993 issue of the Journal of Clinical Psychiatry. By that time, hundreds of patients had already been rescued from the under-treatment that still comprises the standard approach to hypothyroidism in the U.S..
T3 is at least as important as T4 in All Hypothyroid Patients
The excellent paper in your January 1992 issue, "T3-augmentation of anti-depressant treatment in T4-replaced thyroid patients" (1), and the response by Gelenberg elsewhere (2), support a point I have been trying (mostly unsuccessfully) to make with many journals and practitioners of endocrinology and thyroidology: T4-alone is often not sufficient treatment of any case of hypothyroidism (3).
The successful T3-augmentation of T4-replaced antidepressant-resistant patients half-surprised the authors because, although they have themselves previously documented the importance of T3 in depressed patients (4. Joffe et al, 1985; 5. Cooke, 1990), they still labored under the belief that T4-replaced hypothyroid patients are always adequately treated. They now are open to the idea that depressed hypothyroid patients, at least, may often require combination T4-T3 treatment rather than T4-only treatment. I would go further and suggest that all hypothyroid patients require both their T4 and T3 bloodlevels to be in their mid- to high-normal ranges. If T4-only treatment provides these levels, fine; if not, T3 needs to be added to the treatment.
All the latest authoritative texts on the thyroid gland and the treatment of its underactivity (6. Ingbar, 1985; 7. Ingbar and Braverman, 1986; 8. Utiger, 1989; 9. Greenspan, 1991) point to the great importance of T3 thyroid hormone, and to its 9-times-greater activity, compared to the T4 hormone, which they consider virtually merely a pro-hormone or pre-hormone. But then, when it comes to treatment, they all recommend the sole use of T4 in almost all cases! There are some (both theoretical and practical) reasons for this, at least in the past, but I suggest that, nowadays, with the ready availabilty of the very accurate free-T3 bloodlevel, these arguments no longer hold water. They mainly center around the greater stability of the T4 blood-level, in comparison to the T3 level, which has wider diurnal and post-dose fluctuations. Twice-daily dosage of all preparations containing T3 goes a long way toward removing this objection, which I believe is overblown anyway, even in once-daily dosage regimens.
It is assumed that, except in the 'euthyroid sick syndrome' and certain special situations, such as lithium therapy (10. St Germain, 1987), T4 converts peripherally to T3 in fairly standard amounts and at fairly standard rates. It only takes the consistent measuring of both free-T3 and free-T4 bloodlevels, in all one's hypothyroid patients, every time, to very rapidly dispell this myth. If one believes that both the T3 and T4 hormones need to be in their mid- to high-normal ranges, one soon discovers that, while a certain percentage of hypothyroid patients do convert enough T4 to T3 at a sufficient rate for T4 treatment to be adequate as a source of T3, a substantial proportion of patients require some combination of both exogenous T3 and T4.
The other big double-myth is that (a) an elevated ultrasensitive-TSH level is always required before a diagnosis of hypothyroidism can be made; and that (b) its nearly-complete suppression always means that at-least-adequate treatment is in place. There seem to be subtle failures of TSH response to low thyroid hormone levels that cannot be explained purely by the usual forms of hypopituitarism (with secondary hypothyroidism), or by the euthyroid sick syndrome. Whether we are dealing here with tertiary (hypothalamic) hypothyroidism or with a TSH-specific hypopituitarism or whatever, I suggest that more reliance be placed on the absolute free-T3 and free-T4 levels in both diagnosing and treating hypothyroidism. And the T4 (or total T4), T3-uptake, FTI, 'T7', total T3, and T3-by-RIA tests should be abandoned because they are unreliable as gauges of thyroid function (6, 7, 8, 9). I have observed hundreds of patients whose thyroid status was previously regarded as normal, based on these tests (and sometimes even with a normal TSH level), who are very grateful for the treatment they started receiving when the free-T3, free-T4 and ultrasensitive TSH levels were done exclusively, then sensitively interpreted and responded to.
Using this approach, one does not need to resort to the use of tricks like T3- or T4-augmentation of antidepressants, or argue about which is the better of the two (11. Joffe and Singer, 1990). One merely needs to test sensitively for the presence or absence of grade-1, -2 or -3, primary, secondary or tertiary hypothyroidism (12. Evered et al, 1973; 13. Haggerty and Prange, 1990) and treat it if it exists, whether the patient is depressed or whether the patient has other effects of hypothyroidism, like panic-attacks, chronic fatigue, constipation, very dry skin, hair-loss, impotence (14. Baskin, 1989; 15. Wortsman et al, 1987), unexplained weight-gain, dementia, paranoid psychosis (16. Reed and Bland, 1977; 17. Logothetis, 1963), or whatever - always ensuring that a 'balance' of free-t4 and -T3 is achieved, when possible (ie, when there is no 'euthyroid sick' situation).
Yours faithfully, John V Dommisse, MD, FRCPC References
For the complete explanation of this dynamic approach to hypothyroidism, in the form of a full-scale copyrighted medical journal article, go to the Order page at the end of the main website and order Natural Medicine Letter #8 (for $10).
For the abstract of this paper,
Or, for a detailed narrative explanation of this approach to hypothyroidism, see the long interview with me by Mary Shomon on
|
|||||||
Footer TextHome
| Biography | Scientific
Publications | Memberships, Honors &
Awards | Tucson, AZ 85750-1822, U.S.A. Email: John@JohnDommisseMD.com Phone number: 520-577-1940 Fax number: 520-577-1743 |
|||||||
'FREE NEWSLETTER AND PLENTY OF INFORMATION 