Contact: Mike Houghton, telephone 01244 378276 or e-mail Mike@chestermesh.org.uk

ME and The Thyroid Gland

Dr Gordon Skinner

Based on a talk given to Chester MESH 20th June 1997

How I got interested in all this

It used to be thought that ME was associated with a chronic virus infection and in my role as a virologist I was sent patients suspected as having ME largely on the basis that we would deal with their chronic infection. It seemed to me after a while that by and large there were very few patients in which I could identify a source chronic virus infection and so I started looking elsewhere.

About 5 years ago a patient came to me who gave the appearance of being hypothyroid but when I did a thyroid chemistry analysis it was absolutely normal. I discussed this with the patient’s family practitioner, who was also at a loss as how to proceed. It would have helped if we had read the old text books, because in the olden days there weren’t any laboratory tests and people had to proceed on what they saw and heard. Finally after a lot of coming and going and severe trepidation, we did cautiously treat this lady for an underactive thyroid and she was completely cured.

So that fired me in an another direction asking essentially how many patients with ME had got something which was curable.

Possible causes of thyroid malfunction

I have compiled some statistics on the patients in whom we have identified a precipitating cause:

50% of patients have a history of an infectious episode, most usually glandular fever, but it can be a sore throat, influenza, (influenza B seems to be particularly troublesome), food poisoning or gastro enteritis.

About 20% appeared to suffer an initial trauma. For example, a bad childbirth (bad in the sense of prolonged labour, loosing too much blood or a difficult delivery); motor car accident seems peculiarly common particularly if there is neck or spine injury. One chap was assaulted and became ill.

The trauma can be emotional, very commonly a bereavement or marital or partner dissolution. One man collapsed when he was telephoning from a call box; one teenager had mercury poisoning (strangely from having bitten a thermometer in the mouth); one chap seemed to develop symptoms of ME after an alcoholic binge one weekend; and two patients, seemed to be in reasonably in good health until they did that extraordinarily ill-advised thing of running a marathon and I think it simply overloaded the system.

I would suspect these were initiating causes, although it is possible the patient was already susceptible to ME and was just tipped over the balance.

Diagnoses within ME

I thought that it would be of interest to give a broad picture of the kinds of diagnoses that I have come across in the course of seeing ME patients over 4 or 5 years. By and large the most common thing has been an endocrine upset, and within this an underactive thyroid gland. Outside of endocrine upsets, the next most common problem has been an anaemia, usually iron deficient but sometimes B12 deficient anaemia. Some patients have genuine psychiatric upset and some do have an infection, most likely chronic hepatitis C, and the symptoms and signs of hepatitis C are very similar to ME. One patient had chronic hepatitis B, two patients had TB and one patient had Aids, so one had to be ever alert. One patient was actually a malingerer and was caught playing football !

Thankfully (and this is one of the shadows that hang over people diagnosed as having ME) none of the patients have had a malignant disease. The ones you are always concerned about are Hodgkin’s disease and leukaemias in young adults, and even the possibility of a secret drug addiction.

The Study

Of the 91 patients diagnosed with ME that I have diagnosed as being hypothyroid, 66 have responded well to thyroxine and are continuing to respond. That leaves 25 patients who haven’t responded, of these 7 were patients who needed to have cortisol (this is the hormone that the adrenal glands produce) as well as thyroxine. I wouldn’t go so far as to say that they had all got Addison’s disease which is the formal name for severe lack of adrenal function but they seemed to have under-activity of the adrenal gland and they have required both cortisol and thyroxine. Dr Durrant-Peatfield believes that pretty well every patient who is deemed to be hypothyroid should also have cortisol supplementation and he gives very reasonable reasons why that should be. I personally haven’t found it necessary in every patient and if it isn’t necessary, my general view is don’t do it. These seven, in my judgement, after a few weeks on thyroxine were not reacting as I had expected. Cortisol plasma readings are not normally measured because of financial constraints so I use a bit of judgement. If there is low blood pressure or if the patient has an unexplainable yellowish tint to their skin or a lot of dizziness or if they tend to have cold hands and cold feet these are signs often of adrenal insufficiency.

The next thing that it is critical to exclude is diabetes. Everyone, whether or not they have ME should test their urine with Clinistix ­ if positive it should be further investigated. Diabetes is easily treated but catastrophic to miss. Other indicators of diabetes are family history, thirst and dry mouth (also present in hypothyroidism and ME), going to the loo too often, recurrent yeast infections, itchiness and tiredness. One of the great problems is that there are about 20 illnesses that all present with tiredness.

Three patients have turned out to have Cushing’s Syndrome. This is the opposite of Addison’s, when there is too much steroid being produced. Again patients usually present feeling fatigued, they tend to be rather obese, they bruise easily, have red streaks on their abdomen, flushed red faces sometimes and they are producing too much cortisol. An important point I would like to make, there were two patients who were thought to have ME mainly on the grounds of fatigue and headache and various other things turned out simply to be hypertensive. I think this is a matter that is not given sufficient attention. In other words blood pressure was too high and no one was doing anything about it. These were in a sense missed diagnoses.

A few patients have stopped taking thyroxine, resulting from the return of symptoms which they have had before treatment. That is a difficult situation particularly if you are working from afar because you need to see the patients and talk to them to discover why they have decided not to take the thyroxine. Sometimes it’s because they have been told ‘you’ll have a heart attack or your bones will break’.

Four patients I think have a genuine psychiatric upset; some patients get tremendously angry at this diagnosis, it’s not a grave insult, there’s no shame in developing a psychiatric problem. One patient had anorexia nervosa, who is now completely cured by her psychiatric attendance.

Three patients, I don’t know what is wrong with them. None of these three are awfully unwell, two seem to have intractable obesity. These do not appear to be hypothyroid and they certainly don’t respond even to large doses of thyroxine but none the less remain obese, even though they diet. I think this may be a problem that the profession hasn’t looked into.

Explanation of study done by Dr Skinner, Diana Holmes and Afshan Ahmed

This took patients with ME, who by and large responded to thyroxine treatment and measured their FT4 levels, that is the free thyroxine (a lot of laboratories don’t measure this which is a pain).

The graph plots their FT4 readings on the left compared with healthy volunteers on the right. The first conclusion is that the FT4 level of healthy people is higher than the FT4 level of people with ME. What is also interesting is that the lowest normal level in a healthy person is 13.5 and the average is about 17. However, in ME patients the average is 12 and the highest is about 14, so that tells you that patients with ME have a significantly lower level of free thyroxine. There will be exceptions, a few ME patients have a higher level than a few of the healthy people, that’s the way biology works. It is obvious from this chart that the ‘reference intervals’ should not be used alone in diagnosis. The reference interval most laboratories use is 10 ­ 20. The interesting thing is that all the patients who I diagnosed as hypothyroid are within it. My conclusion would be that unless there is some other incredible interpretation, if you have a value between 10 and 13 you may well be hypothyroid. However, looking at it reversely, if you have a value over 16 and I have found this in practice, you will generally not respond to thyroxine treatment, which makes sense. So the FT4 has a value but interpretation is often haywire at this present moment. If you follow the most traditional rules all the people on the chart between 10 and 20 would not be treated.

This chart plots the Thyroid Stimulating hormone. The TSH works the other way round, the higher it is the more likely it is that the patient has a thyroid problem, because the TSH drives on the thyroid; low thyroid activity means a high TSH reading. What is interesting here is that we get the reverse situation. These healthy volunteers have an average of about one; the ME patients have an average of about 2.7. In summary you can say they have a significantly higher TSH and significantly lower thyroxine level. One of the very important features of this is that some hypothyroid or hypothyroid ME patients are under 2 and some under 1. If a laboratory only measures the TSH of these patients they will be diagnosed as ‘falling within normal range’ unless symptoms are considered. These numbers throw into grave doubt the present interpretation of these tests.

What are the dangers of giving patients thyroxine?

Yes, thyroxine is dangerous in that if a patient swallows a whole bottle of thyroxine they might die. If you take 20 pints of water you’ll drown. So any substance on this earth if taken in too high an amount will kill you. Now unless the patient is deranged and the doctor is deranged, that is not going to happen. In the past people used to be given massive amounts to lose weight which was ludicrous. Any reasonably controlled regime, and I think myself I am inclined to veer on the cautious side, will not give you heart problems or osteoporosis. You are after all only trying to achieve normal levels for that patient and if normal levels led to problems the whole world would be having them.

What some of my colleagues confuse patients with is by forecasting the problems of a chronic high overdosage. But long before it reaches this stage the patient will come and say I don’t feel right, I’m getting hot and sweaty and my pulse is going too fast and, unless the patient has not been informed of what to look out for, they’ll say reduce the dosage, so the whole problem is a little contrived. I have never in my professional career seen a problem arising from thyroxine replacement under reasonable conditions.

Now why doesn’t thyroxine work sometimes?

Apart from mis-diagnoses, the usual problem is that the patient is not getting enough of it. Sometimes as the results move up, say from 9 to 12, some of my colleagues will either stop the treatment or they won’t increase it, saying the patient is normal now. It is considered correct to get the level somewhere towards the upper end of the reference interval. The other thing apart from the dosage is time, the longer a patient is on it the more they remove mucopolysaccharides from the body the more the whole body gets into tune again.

Sometimes patients get impatient and decide to try something else and essentially they just haven’t given it enough time.

Sometimes you get a conversion problem where it can be useful to use FT3 as well as FT4.

Sometimes some people are strong adherents of natural thyroid which comes from a pig and of course contains all the hormones of the thyroid gland. This is useful particularly with patients that have had the thyroid removed or killed with radiation for being overactive because in these patients they may have lost all their hormones. There’s various hormones in the thyroid gland, there’s parathyroid, there’s calcitonin and there may be things we don’t know about, so it makes sense to restore the whole lot.

Finally of course the thyroxine may not be operating properly in the cells and a number of people, including Dr Peatfield, think that cortisone supplements may allow it to be utilised properly.

Dr Gordon Skinner DSc, MD (Hons), FRCPath, FRCOG

Dr Gordon Skinner can be contacted at:

Harborough Banks
Old Warwick Road
Lapworth
Solihull
B94 6LD

Tel 01564 782488

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