Oct 2023 report says that to avoid heart problems in later life keep TSH and Free T4 at these levels; please advise if this is correct?

[melodie]

sciencedirect.com/science/a....

The findings from checking patient records is that the lowest risk of heart disease in elderly people is when they have:

Free T4 between 13.5 -14.8 pmol/L

TSH between 1.9 - 2.9 mIU/L

Can anyone better versed in interpreting medical language please assist as this is as far as I got and any additional input would be greatly appreciated

[tattybogle]

Hi melodie, just a heads up , you've copied the TSH / fT4 results wrong way round. You can edit post by clicking on 'more' .

It's a paper i haven't read yet ... will have a proper look at it another day and reply properly ,...... basically it's a balance between risk / quality of life .

Keeping TSH / fT4 at these levels may well give lower statistical risks ... but where we feel best is very individual.... some people would not feel well enough to function properly at those levels . No point taking a dose that might potentially allow you to live a little bit longer if you feel too unwell to function.

[melodie in reply to tattybogle]

Oops, thank you so much. I’ll swap it round now 🙏

[jimh111]

I think you got your TSH and fT4 figures crossed. I'd need to get the full paper but this is consistent with lower than average fT4 being associated with longer life but in general a slightly higher TSH usually gives a longer life. A high normal fT4 is associated with mortality risk and perhaps a higher TSH reflects lower fT4 levels.

[Noelnoel in reply to jimh111]

So what’s the “average” FT4

[jimh111 in reply to Noelnoel]

There are various studies that measure quartiles or tertiles risks. The distribution of TSH is a little asymmetric so the median level is just above the middle of the reference interval. So, with a typical fT4 reference interval of 10.0 - 22.0 an average would be around 16.5.You have to be careful because the results depend on how the researchers decide to group the study groups. In general higher fT4 levels carry increasing risks.

[Noelnoel in reply to jimh111]

Thank you

Mine’s stubbornly too low but I’m working on raising it a little

[Sparklingsunshine]

I see there's no mention of FT3 levels, the problem being that in order to get decent FT3 levels some Levo users have to take high doses of Levo that suppress TSH and give them high FT4 levels. Which is not ideal but as the NHS is generally anti T3 what else can they do?

[MissGrace in reply to Sparklingsunshine]

Nail on the head. Treating Levo replacement as if it is the same as the workings of a natural thyroid and is metabolised in the same way through the stomach is a blight on all of us. 🤸🏿‍♀️🥛

[Sparklingsunshine in reply to MissGrace]

I'm one of them, last year I was taking 150mcg of Levo, my FT4 reached the giddy heights of 13 and my FT3 was 3.6, whereas I'm now on 200mcg and have an FT4 which is top of the range but it has pulled my FT3 to 5.2, still not optimal but better. ( range FT4 12-22, FT3 3.1 -6.8) .

Its not ideal and I'm not chuffed about the risks but as Humanbean rightly says quality of life now is more important than potential problems later, which might never happen.

[humanbean]

One major point I would make about this research is that the data they used came from people without overt thyroid disease.

In the Methods section (my emphasis) :

This systematic review and individual participant data (IPD) meta-analysis identified eligible prospective cohorts through the Thyroid Studies Collaboration, supplemented with a systematic search via Embase, MEDLINE (Ovid), Web of science, the Cochrane Central Register of Controlled Trials, and Google Scholar from Jan 1, 2011, to Feb 12, 2017 with an updated search to Oct 13, 2022 (cohorts found in the second search were not included in the IPD). We included cohorts that collected TSH or FT4, and cardiovascular outcomes or mortality for adults (aged ≥18 years). We excluded cohorts that included solely pregnant women, individuals with overt thyroid diseases, and individuals with cardiovascular disease. We contacted the study investigators of eligible cohorts to provide IPD on demographics, TSH, FT4, thyroid peroxidase antibodies, history of cardiovascular disease and risk factors, medication use, cardiovascular disease events, cardiovascular disease mortality, and all-cause mortality.

Excluding people with thyroid disease matters a lot. Imagine a healthy person with a healthy thyroid. Their thyroid will produce thyroxine (T4) in spurts all day long (I've seen the word "pulsatile" used to describe thyroxine production.) T3 will be produced as necessary, in spurts all day long. (But they never bothered to measure T3, the active thyroid hormone, which I think is a massive flaw in so much thyroid-related research.

Then compare that to people who have thyroid disease, either hypothyroidism or hyperthyroidism. In the case of hypothyroidism most patients will take one or more T4 pills per day, and the patient's levels will make one or more jumps throughout the day. Ditto with T3 if the patient takes it.

The production of T4 and T3 in patients with hyperthyroidism will be totally different to someone who is healthy with a healthy thyroid.

Someone who has thyroid disease of any kind is likely to have a higher rate of heart disease than a healthy person, because thyroid hormone levels affect the heart.

If anyone was to use this research as proof I must have my TSH higher than I currently keep it, and my Free T4 and Free T3 must be lower, then as far as I'm concerned they can go and take a long run off a short pier.

If I want to prioritise my quality of life over my quantity of life that is my decision, and doctors should allow me to decide for myself on that score.

[melodie in reply to humanbean]

Well spotted Human Bean 👏

[tattybogle]

Good to see this bit acknowledged :

"Most guidelines of subclinical hypothyroidism (elevated TSH combination with FT4 within the reference range) recommend treatment when TSH is greater than 10 mIU/L given the increased risk of cardiovascular disease , as well as progression to overt hypothyroidism. However, TSH concentrations lower than currently used treatment thresholds are already associated with a higher risk of fatal coronary heart disease."

So far so good . sub clinical hypo has increased risks long before TSH gets up to 10 .

But note , the study is looking at people with no thyroid disease / not taking thyroid hormone replacement . So it's conclusions about TSH/ risk can be applied to diagnosis of untreated sub-clinical hypo patients.

But they then suggest the fT4/ TSH results can be applied to clinical decision making (dose adjustments) for patients already taking levo..... they can't .

Taking replacement thyroid hormone alters the relationship/ ratio of TSH / fT4 / fT3 .

you get a relatively lower TSH for a relatively higher fT4 .. with relatively lower fT3 .

So the results / conclusions from these studies of people without thyroid disease cannot be directly applied to treated thyroid patients .

[melodie in reply to tattybogle]

Very good to know 🙏