The use of levo-thyroxine (called Eltroxin in UK, and Synthroid in USA) is considered by most physicians to be the only treatment on the table. A number of generic brands are now available, but some patients and doctors have found they lack consistent efficiency. It comes as tiny white tablets of 25, 50 and 100 micrograms (mcg). It is always sensible to start with the lowest dose, especially in the elderly; so common practice is to start with 25 mcg. This may be increased in increments, up to a dose regarded as standard of 100mcg. At this point most physicians stay their hand, and the patient may have to remain on this dose until kingdom come, with any changes of dose decided by blood test exclusively, little regard often being paid to how the patient actually feels.

The problem with this is that it takes no account of low adrenal reserve or conversion blocks, or receptor uptake insufficiency. Also this is not the way nature does it. As we saw earlier, thyroid hormone is 80% thyroxine, 17% tri-iodothyronine, and the remainder T2 and T1. The fact that patients with non-severe thyroid sufficiency manage on T4 alone is no credit to the physicians. If the condition is not too far advanced or of too long standing, all the thyroxine (T4) will be converted to tertroxin (T3) and used with consequent patient benefit. Sadly, many endocrinologists refuse to accept that supplementing thyroid hormone, the way nature does it is necessary or desirable, mostly on the grounds that they know best. I must tell you now that, except for mild early cases, this is not the best way to provide thyroid supplementation.

The more serious thyroid deficiency will respond only poorly to this regime, since it takes no account of the adrenal connection, conversion block, or receptor uptake resistance. The patient may feel an initial benefit, but within days or weeks this may wear off; or the patient may soon start to become aware of tremors and palpitations. The blood test may well show the presence of too much thyroid in the blood – since it is not being used – and the dosage will be reduced. This makes the side effects better but the exhaustion and fluid retention and all the other symptoms will still be there, poorly relieved, if at all. It is this situation that I found in about 70% of the patients (already on treatment) I saw for the first time. The conclusion is obvious: for the very large number of patients, thyroxine may only work very poorly or not at all for the reasons we discussed. But even if these problems are dealt with the response may still be disappointing. So we need to consider other options.

The first is to understand that the 5-deiodinase enzymes carrying out the T4 to T3 conversion may be quite deficient or not even work at all. The build up of unused T4 is then inevitable, and within a relatively short time there may be toxic levels present with palpitations, a general lack of well-being, stomach upsets and so on. It may well be quite impossible to predict that this is going to happen, which is why it is necessary to start the treatment in a standard way, the patient doing the monitoring on a daily basis: pulse and temperature, am and pm, and perhaps something like a 1 to 10 feel good factor, all written down daily. If symptoms occur and things are not right, the thyroid is discontinued, but everything else remains in place, including the adrenal support. When the coast is clear, say in 7 to 10 days, one or two alternatives may now be used. Using thyroid supplementation obtainable from your doctor on prescription, we may use the already converted thyroid hormone, the liothyronine (T3). This is marketed in the UK as Tertroxin, 20mcg tablets and in the USA as Cytomel, 25mcg tablets.

The T3 is the active thyroid hormone that actually does the work of controlling metabolism. It has two important differences from thyroxine. Firstly, it is rapidly metabolised, having a half-life of about 1 . 5 to 2 days and the effect lasts for about 8 hours, unlike thyroxine, which has a half life of around 7/8 days. So the blood levels decline rapidly at first and then more slowly, but some remains for some time. In practical terms though, there is pretty well no T3 left worth talking after about 24 hours or so. This is unlike T4, which takes time to build up its levels in the bloodstream and 3 or 4 weeks at least for the amount in the blood to drop below a therapeutically effective level. This means that T3 works a good deal quicker than T4.

The second difference is that microgram for microgram T3 is a good deal more powerful than thyroxine; something like five times stronger. So the amount given is proportionately less; and in general 20 mcg of T3 is considered the equivalent to 100mcg of T4

Start the dose of T3 at x 20 mcg tablet daily, certainly before midday. After five days or so, the dose may be increased subject to your careful monitoring. Authorities are undecided as to whether the dose is better split into two, or given all at once in the morning; best probably to decide yourself but evening is not a good time since then it is likely to interfere with sleep.

As time goes on the overall dose may be increased, allowing plenty of time to decide how it is all going, by small increments: say a tablet at a time. After decided improvement and probably not sooner than eight weeks, it may be possible to substitute T4 for at least one dose of T3, because the conversion problem may be easing. It is perfectly possible to stay on T3 alone, permanently, and many patients have to. The important thing is to keep a flexible approach and not be afraid to experiment; so long as it is all monitored, then you can be sure of what is doing what. The ultimate dose should be whatever suits you best; it may be, for example, T3 and T4, or of one and of the other, or any other variation that works.