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Thyroxine Resistant Hypometabolism (T4 Conversion Block)

You need to copy out two documents to show your medical practitioners, the one below, and the one you will find in our News Section in the right hand column on our Home Page entitled ‘Are you are Victim’ “Reducing the Scope of Guidelines and Policy Statements on Hypothyroidism”. This is something that is not included in the Teaching Curriculum by the Royal College of Physicians nor is it in the Curriculum by the GMC when teaching endocrinologists. 85% of patients do well on levothyroxine, because they are suffering with primary hypothyroidism (insufficient secretion of hormone by the thyroid GLAND) so T4 works well. However, the other 15% (300,000 citizens in the UK alone) are NOT suffering with primary hypothyroidism because their thyroid gland is secreting sufficient thyroid hormone and therefore, their blood results are normal. These patients continue to suffer the same symptoms of hypothyroidism, but they are ignored. They should be treated with T3 and NOT T4. They are suffering with Thyroxine Resistant Hypometabolism. Please make your medical practitioners aware of this, because if they ignore them, they are causing serious harm to their patients.


Euthyroid Hypometabolism – T4 Conversion Block
By Dr Barry Peatfield

http://tpauk.com/images/bank/dr-barry-peatfield.jpg” align=”left” border=”0″ hspace=”6″ vspace=”2″ alt=””/>Euthyroid hypometabolism can, effectively, mean one of two things. Either you have the symptoms of hypothyroidism, but normal blood tests, or you have abnormal blood tests, but one actually feels perfectly well. The last definition we can probably dispose of fairly quickly, since people like this are very uncommon. When you get down to it, they turn out to be positive uncomplaining souls, who sooner or later do start noticing symptoms. And sometimes the tests are faulty, of course.

Its the first definition that we are going to worry about. Folk with this problem are clearly unwell, with all the symptoms of hypometabolism. Their hypometabolic state is due to the fact that the active thyroid hormone, liothyronine, or T3, is not reaching the tissues properly.

This failure has a number of possible causes:

  1. There is insufficient T4 from which to make the T3. This of course is the standard form of hypothyroidism.

  2. There is enough T3, but the tissue receptors are blunted from disuse, and wont take up the T3.
  3. Of the various causes of insufficient T4 there are many, and have been discussed elsewhere, and you should be familiar with them. Tests may suggest there is enough available T4, even though the patient is clearly hypothyroid. This is what people mostly mean when they talk about euthyroid hypometabolism. Youre ill, but tests are normal. So what tests? The standard TSH and T4 are less than satisfactory; the only hint you might get is from a markedly elevated T4. As we know, doctors wont usually ask the lab to do the T3 even at gunpoint; but sometimes they do, and the low T3, and high T4, will tell us whats going on. TSH may be quite low, because of the raised T4.

    Unforgivably these days the clinical history may be too brief, and perhaps, therefore, unhelpful, and, sadly, no proper examination is made. The fact is, that a wealth of evidence may be obtained from a proper clinical examination, and a diagnosis made on that basis alone. Yet this, all so often, is not, the way its done. The signs of a low metabolic state are invariably there for simple inspection; so that, in spite of apparently normal, but inadequate, test results, it is perfectly clear that the patient has a low metabolism, and the right tests havent been done to demonstrate it. I think that to use the term euthyroid hypometabolism is inappropriate; its simply that the diagnosis hasnt been made properly. Euthyroid means normal thyroid and you know youre not right.

    So, apart from a decent clinical appraisal, what should we have done to test for the condition. As I said the serum T4 and T3 will provide some indication, since there is likely to be a normal, or elevated T4, and the T3 may be low, out of range, or at the lower end of the range. The TSH may be low, if the T4 is high, and give rise to the impression that there is thyroid hormone in plenty. There may very well be; but the system cant process it properly, so that you can be hypothyroid in, as it were, the midst of plenty. The more satisfactory thyroid test is the 24 hour urinary thyroid hormone, which the NHS wont do. This test is widely used in the USA and much of Europe; in the UK it can only be arranged by private request. You are sent a pot of your own to pee in over 24 hours; and a syringe to sample a small amount, which you send back to the lab. They measure how much thyroxine you have made (or is available from treatment) in 24 hours, and how much you converted to T3. A common finding is high T4 levels but low T3, which certainly gives the whole thing away. If T3 is normal, this will mean receptor resistance (also helped by adrenal support).

    The other useful test is the Adrenal Stress Profile. Since the conversion enzymes that do the conversion of T4 to T3, need adrenal hormones as co-factors to remove the 4th iodine atom from thyroxine (T4), and thus leave 3 iodine atoms only, then it follows that weak adrenal function means the conversion wont occur normally. (Just be reminded that the 5deiodinase conversion enzymes sometimes lose their function anyway, even if adrenal glands are actually functioning okay.) The serum cortisol and Synacthen test are used sometimes, but are usually misinterpreted, and come back as normal.

    Low T3 over 24 hours, or low T3 and high T4 serum tests, and low adrenal function make the T4 to T3 conversion failure obvious. You then have the explanation for the conversion block, with okay T4 levels, okay TSH levels, but the patient still obviously hypothyroid. Whether euthyroid metabolism is the right descriptive term for this state of affairs, I rather doubt; and it can be confused with the other form of euthyroid hypometabolism described earlier. We should describe this as failure of T4 conversion, or thyroxine resistant hypometabolism.

    Treatment

    Mild to moderate conversion block will often respond to supporting adrenal function. This can be done nutritionally, with supplements. Extra vitamin C, Co-enzyme Q10 (ubiquinol), B12, iron, vitamin D, iodine, all support adrenal function. If adrenal gland function is really not very good, I like to use natural adrenal glandular cortex preparations, for example, Nutri Adrenal Extra, or Nutri Adrenal. Most often these restart adrenal function and activity, so that the conversion enzymes start to work, and make T3 from the T4, as they are meant to. I make sure adrenal function is supported as well as it can be. Rarely, bioidentical cortisone and DHEA may be needed.

    But, after years of illness and especially after thyroid ablation this wont be enough. Then the active, converted, thyroid hormone is required. This is liothyronine, or T3.

    For reasons that defy explanation, the Royal Colleges discourage the prescription of liothyronine (T3), so that doctors wont prescribe it even at knife point. The American version of T3 (Cynomel and Cytomel) are really excellent, and are 25 mcg as opposed to the UKs 20 mcg liothyronine. Personally, I think they are better preparations, than liothyronine, but, of course, you have to pay for them.

    The dose starts small, and builds up gradually, with the thyroxine, synthetic or natural, being reduced, sometimes to zero. Watch is kept on pulse rates, temperature, symptoms, every few days, and the amount of T3 adjusted accordingly.

    One important point about this, is that the levothyroxine (T4) or even Armour (T4 & T3) or other natural thyroid will need to be reduced as the T3 is given, since the extra may prove simply too much, and overload things.

    Doctors and the Royal Colleges seem increasingly reluctant to consider the use of T3 at present. They have convinced themselves that T3 is somehow bad for the heart, or may cause osteoporosis. This is a disgrace, and ridiculous. You would have to be taking very high doses of T3, and there would, very quickly (especially if monitoring yourself) be obvious side effects that you couldnt ignore, long before damage would occur.

    We all, you and me, actually run on T3; thyroxine is no good at all if it doesnt get converted to T3. The conversion failure, and build up of unused T4 that results, causes toxicity heart problems and osteoporosis. So its the other way around. Trying to cram more T4 into the low thyroid patient simply causes all sorts of toxic symptoms and chronic illness. Of course overdose of T3 will cause a problem, as with any medicine but no more than overdosing with T4.

    I am often asked what causes the conversion failure in the first place, so well look at this.

    • Prolonged thyroid deficiency illness, especially where the replacement treatment hasnt been satisfactory.

    • A genetic predisposition to 5deiodinase failure.

    • Thyroid ablation (surgery or radioactive treatment) seems to eventually result in conversion failure.

    • The older age groups.

    • Adrenal stress and eventual fatigue.

    This latter is quite common, but the conversion picks up again when the adrenal dysfunction is treated. This is much the most common scenario, and treatment of the adrenal glands should be done first. If improvement is marginal, then additional T3 should be used.

    Receptor resistance. Even with adrenal help, receptors may be blunted from disuse, or inappropriate treatment, and patience and care have to be used to build up the dose of T3 gradually.

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