Most of us already knew this but it has been confirmed

[shaws]

This is from TUK and read the first topic.

thyroiduk.org.uk/tuk/newspa...

[Scazzoh]

So 'biochemical euthyroidism' cannot always be achieved with T4 hormone replacement as there are 'subtleties that have only recently been recognised by the medical community'. When is it going to start listening, acting and given people a choice of treatment depending on their symptoms?

[shaws Administrator in reply to Scazzoh]

Those who should be at the forefront of treatment I doubt they read or take notice of research. Of course, they don't want to be seen to be unknowledgeable but still insist on levo alone is the only treatment. Some members have had horrible unsympathetic appointments with some of them.

I agree with you that if people are suffering on levothyroxine alone, at least they should offer alternatives on a trial. The BTA and the RCoP ignored the following re NDT and stick to their guns while we know many on this forum have recovered their health. Despite 3 yearly reminders, neither responded to Dr L before his untimely death:-

thyroidscience.com/Criticis...

[jimh111]

This is an interesting paper that shows up small differences. It is a retrospective study from the NHANES data. It is important to note that there were two sets of controls, the first being all subjects who were not on L-T4 which included a greater proportion of males and younger people. The 'matched controls' were matched for age, sex, race and TSH levels. This group gives a fair comparison.

Compared with the matched controls the patient group:-

Had a higher BMI: 29.8 re 28.2. I'm not sure this is a reflection of the treatment or not. We all know that once you are hypothyroid and put on weight it is very difficult to get back to your original weight. I suspect the higher BMI is partly due to L-T4 only treatment and partly due to delays in diagnosis.

Cholesterol and lipids were a little higher in the patient group. We know a little L-T3 helps resolve this.

The patient group had more use of beta blockers, statins and anti-depressants. I wonder if this is in part due to increased attention to these issues in hypothyroid patients and partly due to issues brought on by the lack of T3.

The patient group had a lot less 'Metabolic equivalents', i.e. exercise, both at work and recreational - only two thirds as active as matched controls. This is a much greater concern. Is it in part due to poorer health or are hypothyroid patients conditioned to lower exercise expectations? I suspect the subtle cognitive impairments associated with L-T4 only therapy have a profound effect on the desire and confidence to engage in exercise.

Remember this patient group are those prescribed L-T4 and will constist of patients diagnosed with primary hypothyroidism based on guidelines regarding TSH. This study does not include those of us on these forums who may have more serious conditions and are misdiagnosed with ME/CFS or whatever (if diagnosed at all). The reduced activity levels will have an effect on the prescribing of statins, beta-blockers and anti-depressants. They studied patients in the USA, patients in other countries may have different profiles and behaviour.

In my view the most important point this study raises is that there was no association with the patients' symptoms and fT3, fT4 or fT3 / fT4 ratio. Of course giving extra T3 might improve matters but the symptoms were not related to mildly low levels of T3. This suggests a 'TFT independant' factor, perhaps a form of peripheral hormone resistance. i.e. there is selection bias when diagnosing primary hypothyroidism. If two subjects have the same marginal levels of TSH, fT3 and fT4 the one with hypothyroid signs and symptoms will be (mis)diagnosed with primary hypothyroidism. Their hypothyrodism has nothing to do with their mildly elevated TSH but they have been consigned to the primary hypothyroid cohort.

[jimh111]

This study found that there was no link between the fT3 / fT4 ratio and symptoms. The patients will have been diagnosed with primary hypothyroidism due to whatever cause and medicated with levothyroxine.

There clearly is a large body of patients with hypothyroidism that is not caused solely by a failing thyroid gland who wrongly receive a diagnosis of primary hypothyriodism or no diagnosis at all. These patients usually require substantial doses of T3 medication, their individual fT3 / fT4 ratio will be drastically different to the general population.

fT3 / fT4 ratio is meaningless. In healthy people the ratio varies as fT3 and fT4 drift up and down. As a patient's thyroid gland starts to fail TSH rises, fT4 falls and fT3 remains reasonably stable (or even rises a little) until there is too little T4 to convert to T3. i.e. in mild hypothyroidism the fT3 / fT4 ratio is higher (or fT4 / fT3 ratio lower).

If fT3 and fT4 are in the upper part of the interval the fT3 / fT4 ratio can be the same as in a hypothyroid patient with fT3, fT4 bouncing along the floor of the reference intervals.

Taken by itself fT3 / fT4 ratio does not illuminate the status of the patient. It can be useful to look at the relationship between TSH, fT3 and fT4. For example high TSH, highish fT4 and low fT3 could be due to impaired deiodinase.

[diogenes Remembering]

The study is not well performed unfortunately. As always patients were mixed up according to how much thyroid they had left and this confounds the analysis. We're in the process of analysing and writing up a study that concentrates on patients with no thyroid (athyreotic). The patients on T4 only have been coming in over a period of 3-8 years so there are multiple readings for each of 322 patients. 2950 results in all with TSH, FT4 and FT3. We agree that the FT4/FT3 ratio doesn't change whether patients have complaints over treatment or not. So it isn't the rate of production of T3 from T4 that is important. But we find a significant inverse relation between complaints and FT3 level - that is the lower the level the more the complaints as you'd expect. We too are confounded somewhat in that the patients comprise a group ranging from the good to the poor converters, but we remove a further confounding factor of residual thyroid function. So unlike the rate of conversion, it's the concentration of the end product T3 that determines complaints. This is a retrospective study whose information we dragged out of the hospital archives without really knowing what we'd find. However it confirms and adds to all we've so far said.

[Ruthi in reply to diogenes]

So Diogenes, some of the patients with lower T3 would be good converters on inadequate replacement, and some would be poor converters?

Did complaints correlate with TSH?

[diogenes Remembering in reply to Ruthi]

No

[diogenes Remembering in reply to Ruthi]

Just to add that we did try to separate good, medium and poor converters according to their FT4/FT3 ratio on T4 alone and this seems to show the poorer converters to have the greater incidence of complaint.

[Ruthi in reply to diogenes]

With post TT pets, you obviously can't look at measures on first complaint. Were there any notable differences according to age, gender, length of time post TT?

And with your research on set points are you following people to see if some are more prone to thyroid disease than others?

[diogenes Remembering in reply to Ruthi]

Sorry I should amend my no into a yes re TSH. I got mixed up with TSH's being in normal range or not. Whether complaining or not they actually are at or below the limits of the normal range. For non complainers the TSH range was 0.07-0.08 and for complainers 0.14-0.19. So though TSH entering or leaving the normal range was not relevant, the TSH's were different on average and significantly higher for complainers.

[Ruthi in reply to diogenes]

So waht about all those poor people who are kept with their TSH well above 1?

[diogenes Remembering in reply to Ruthi]

Some (the good converters) may be OK, the average people should be 1 or less, and the poor converters small down to nearly undetectable. BUT the healthy normal range isn't suitable for any of these and should be reduced for those on therapy generally.

[diogenes Remembering in reply to Ruthi]

I also should mention that BOTH T4 and T3 control TSH production by the pituitary. Up till now it's assumed that T4 has the major role. Well that's true if you think that 60/40 T4/T3 is a minor role for T3.

[diogenes Remembering]

Age, body mass all have an effect on the results. Not gender, not length of time post thyroid loss. We're not proposing a prospective trial as such, because this would need considerable bureaucracy and cost to st up which we can't afford. However we can continue to followup those patients mentioned in the analysis.