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The Safe and Effective Prescribing of Thyroid Hormones:
Guidelines for Doctors

Convenor: Dr Sarah Myhill for the Thyroid Special Interest Group of the British Society for Ecological Medicine


The British Thyroid Foundation (BTF News magazine - Issue no 67 Winter 2008/2009) and more recently the Royal College of Physicians have issued guidance for prescribing thyroid hormones for primary hypothyroidism which are entirely based on biochemical criteria.

They also recommend solely synthetic thyroxine (T4) as the only acceptable replacement therapy.

These proscriptive guidelines have resulted in enormous patient dissatisfaction and uncertainty for clinicians. Many patients choose, often against medical advice, to increase their dose of thyroid hormones, or swap to biologically identical thyroid hormones because clinically they feel so much better. Our aim as clinicians is to give patients the best possible health and we should be working with them to ensure this while protecting against possible problems associated with overdosing.

The following is a clinical guide to the safe and effective prescribing of thyroid hormones as agreed by practicing physicians within the thyroid special interest group of the BSEM.

Underlying Principles

Patients vary in their biochemical and hormonal requirements as much as they vary in their requirement for food, micronutrients, characters and personalities. No one size fits all. The prescription of thyroid hormones is both a biochemical and a clinical decision – weight must be given to both of these issues. Conventional prescribing guidelines are almost entirely based on biochemical criteria. Problems arise because the individual person’s normal range is not the same as the population normal range and most importantly not necessarily consistent with the laboratory reference ranges.

Reference ranges in individual laboratories will vary. The reason for this is that each new assay is tested against a large batch of stored sera, often obtained from blood donations. These will contain some undiagnosed thyroid disease and so the distribution (creating a bell curve of frequency) will have at its extreme ends people with both hypo and hyperthyroid abnormality but at the time of blood collection, undiscovered. This is one reason why reference ranges are wider than any normal range. Also the population normal ranges will fall well within the reference ranges of any laboratory. The dilemma is knowing clinically how to address someone who has a biochemical result within say 5 – 10% of the edge of the reported reference range.

Furthermore individual normal ranges may be much narrower, running tightly within a few pmol/l – individuals have a genetically set free T4 status. As clinicians we see there is no doubt that some people feel much better running high normal levels of thyroid hormones rather than low normal levels, but remaining within, or just outside, reference ranges.

Who has Hypothyroidism?

Thyroid disease should be suspected clinically from the many clinical symptoms and signs listed in the literature. Any patient with a chronic fatigue syndrome could be hypothyroid. However, clinicians need to be mindful that there are a great many other causes of the symptoms in the literature and signs of allergy, poor nutritional status and toxic stress (from xenobiotics such as heavy metals and pesticides), all need to be addressed as a separate issue. This is where biochemical tests are vital as part of the overall picture of thyroid disease.

Current biochemistry distinguishes the three common types of hypothyroidism we see in clinical practice namely:
  1. Primary hypothyroidism – where the TSH is near to the limits or above the reference range. The free T4 may be low but often is not.
  2. Secondary hypothyroidism – where the TSH is low. The free T4 may be low, but often is not.
  3. Poor conversion of T4 to T3 – where the most active thyroid hormone, i.e. T3, is low.
  4. TSH may be high and the free T4 may be high.
Clinically we often see combinations of the above.

There are likely to be other, as yet undiscovered, biochemical indices related to other iodine containing compounds such as T1and T2. We know this because clinically many patients feel much better taking biologically identical thyroid hormones such as Armour thyroid. Currently the biochemical reasons for this are unclear.

So which patient do we start on thyroid hormones?

Those with symptoms suggestive of hypothyroidism that we cannot explain by nutritional, allergic, or toxic stress (chronic poisoning by heavy metals, pesticides, or other sych xenobiotics) who also have biochemistry which is either overtly abnormal, or results towards the limits of the reference ranges for whom there is scope to prescribe thyroid hormones, with little risk of straying outside the reference ranges.

So what are the reference ranges and how do they relate to normal ranges?

The reference range for the upper limit of TSH in UK is probably set too high. In the USA the threshold for prescribing thyroid hormones has recently been changed to a TSH of <3.0 mIU/L. A TSH at the upper limits of the reference range or low normal levels of free T4 and free T3 are associated with increased risk of many chronic degenerative diseases including cardiovascular disease, insulin resistance, lipid abnormalities, inflammation, obesity, cancer (breast, thyroid, prostate), poor survival in critical illness, poor cognitive function, depression, poor outcome of pregnancy and slow neurodevelopmental progress in babies.

Oddly in some UK laboratories, the target range after prescribing thyroid hormones is a TSH of less than 2.0 and sometimes less than 1.5. We do not see the logic for this restrictive observation. The target range is irrelevant when the patient is on replacement thyroid hormones. The aim is to achieve a good clinical status for the patient. This suggested restrictive target range illustrates the wide range of views in UK about thresholds and targets for prescribing thyroid hormones.

The population reference range for a Free T4 is very variable, with some labs stating a range of 7 – 17 pmol/L, others 12 – 22 pmol/L. The point here is that there is often a twofold difference between the lowest and the highest level of Free T4 within the stated reference range. Therefore there is scope to treat the patient with low levels of Free T4, but stay within or close to the reference range. Remember 5% of the “normal” population will lie outside the reference range.

All our clinical experience of patients presenting with the many symptoms and signs of hypothyroidism who improve with treatment, leads us to suspect that hypothyroidism is much more common than generally stated. Reference ranges are misunderstood because people who could benefit from thyroid hormones are classed as normals even though they are at the limits or within 10% of the limits of the reference ranges.

The present serum biochemistry testing fails to indicate the rate of natural production and consumption of the hormones and has limited use as markers of status. The clinical picture is most important. We do need more sensitive biochemical indicators and some clinicans use urinary excretion indices as markers of sufficient hormone production. This needs further research.

How to start prescribing thyroid hormones

Firstly, the patient must satisfy the clinical criteria for a diagnosis of hypothyroidism, or be clinically euthyroid, but certainly not thyrotoxic. Secondly, there must be biochemical scope for a trial of thyroid hormones. It is important to recognise that this is a trial because in most cases we do not know if we are dealing with a patient whose genetically determined personal normal range is at the bottom or the top end of the population laboratory reference ranges.

The starting dose of thyroid hormones depends on the size and the state of unwellness of the patient. Small unwell patients should be started on just 12.5mcg daily, then increase their dose in 12.5mcg increments every two weeks until they get to 50mcg daily, at which point recheck the biochemistry. If the patient has a low T3 then some will find some benefit from a very small dose of T3 in the morning or twice daily as well as T4 replacement . Presently T3 is provided as a tiny 20 mcgm tablet and a quarter with food twice daily can dramatically improve well being.

Later the T3 may not be needed and as it has a short half life, stopping this after the T4 has stabilised will quickly enable a check to be made to ensure that T4 to T3 conversion continues normally on just T4 therapy. Large and more robust individuals could be started on 50mcg daily and increase in 25mcg every two weeks until they get to 100mcg daily, wait four weeks for blood levels to stabilise and then recheck the biochemistry.

Many patients will fall between the two patients described. So long as the patient does not develop any symptoms or signs of hyperthyroidism, and the patients can be taught to self monitor, then the trial should be continued until they get to their target dose. If signs of thyrotoxicosis develop, this may be due to receptor hypersensitivity (in which case they settle down in a few days), or due to biochemical toxicosis despite the biochemistry being within reference ranges. In these cases the patient’s genetically determined normal range is probably set low and is being exceeded by therapy. In either event, reduce the dose by 12.5-25mcg to relieve symptoms and assess the patient clinically and biochemically at the next convenient appointment.

Once up to the target dose, which may be anything between 25 and 200mcgms of thyroxine (or its equivalent), wait four weeks for blood levels of thyroid hormones to stabilise and then re-check for a free T4, free T3 and TSH, assess things clinically and continue to adjust according to the above parameters.


Once stable on the above regimes, so long as no new symptoms arise, patients should be rechecked clinically and biochemically on an annual basis. Once stable for two to three years, again so long as no new symptoms arise, rechecking can be safely done every two to three years.

However, some patients lose the ability to convert T4 to active T3 and monitoring should always check both these hormones.

Swapping the patient to bio-identical thyroid replacement hormones.

One obvious biochemical reason for swapping to bio-identical hormones is if the patient has high levels of T4, but low levels of T3, i.e. they have poor conversion. This is because the biologically identical hormones contain T3. However, some patients just feel much better on biologically identical hormones – the reason why is not clear, but there are other compounds in biologically identical hormones such as T1 and T2, which may well have biological activity, which then translates into clinical well being.

There are many biologically identical thyroid hormone preparations on the market, but they all amount to the same thing – standardised, dried, whole thyroid extract (from pig thyroid). The stability and keeping qualities are excellent. They have many names such as Armour thyroid, generic thyroid, natural thyroid, Thyroid S, Westhroid and so on. They are classified as Unlicensed Medicines but can legally be prescribed by NHS prescription or private prescription.

60mg of biologically identical hormone is the same thing as 1 grain, which contains 36mcg of T4 and 9mcg of T3. Since T3 is four times more active than T4, the T3 equivalent is 36mcg.

Therefore one grain of natural thyroid is “equivalent” to 72mcg of T4.

Therefore a patient stabilised on 75mcg of synthetic T4 could easily be swapped to one grain of biologically identical hormone. Because T3 has a short half life, this is given in two doses daily.

Monitoring biologically identical hormones

The principles are exactly the same as synthetic thyroid hormones. However, the ratio of T3 to T4 is high for human requirements and so expect the blood tests to show high T3 compared to T4. Because T3 is short acting, levels fluctuate quite markedly over the 24 hours so the time at which the blood test is taken also needs to be taken into account in interpreting the results.

Monitoring the patient who only feels well on high doses of thyroid hormones with a suppressed TSH

Some patients fall into this category and it is this which prevents many doctors from prescribing thyroid hormones in the necessary doses to allow their patients to feel well. Our experience is that many patients suffering from a chronic fatigue syndrome have secondary hypothyroidism. In CFS/ME there is a general suppression of the hypothalamic pituitary adrenal axis. Furthermore it is likely that a decline in the activity of the HPA axis is part of the normal ageing process and therefore we believe the incidence of secondary hypothyroidism in the elderly is likely to be increasing with age. Many doctors are nervous of prescribing thyroid hormones when the TSH is low. However, our view is that so long as levels of Free T4 and Free T3 are adjusted as we describe, and the patient feels well, complications need not arise.

Possible long term complications of thyroid hormones

The two complications most often cited are osteoporosis and heart disease. Three points here.

The first is that hypothyroidism is also a major risk factor for both osteoporosis and heart disease.

Secondly there are excellent nutritional interventions which are highly protective against the development of both osteoporosis and heart disease and the good doctor may wish to consider these in the longer term for the perceived vulnerable patient

The third point, of course, is that unless the patient is feeling well, he/she will be unable to exercise. Exercise is vitally important to protect sufferers from heart disease and osteoporosis.

Properly done, the environmental approach combined with thyroid hormones is an essential tool to protect against chronic degenerative disease.


We are grateful to the International Hormone Society for supplying the references which, being highly technical, we generally reserve for professionals but can be supplied, if requested, to underpin the above prescribing guidelines.

I am grateful to Dr Sarah Myhill for her work and permission to place this on my website and to the BSEM for organising the research group.

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