History of thyroid dysfunction through to treat... - Thyroid UK
History of thyroid dysfunction through to treatment !
Nice article written for thyroiduk by the late (much missed) diogenes ~ also has a link to that video of him speaking at that scottish parliament enquiry thing.
It would appear to be someone in Scandinavia - Sweden or Norway.
Sorry don’t understand?
On the About page:
Mention of Levaxin which is, I think, a levothyroxine brand from Sweden and Norway. I was trying to identify who was behind the site.
a shy Norwegian
Oh ok understand now - the mans name is John Midgley I believe a friend of Thyroid Uk !
helvella - diogenes documents
This document is a tribute to John Midgley - diogenes.
It lists as much of his published work as I have been able to find. Where possible, there are links to accessible copies.
The PDF of this document is here:
dropbox.com/scl/fi/cgnuorpd...
John Midgley was 'diogenes on here , sadly he died last year.
the person running that thyroidopedia site , is someone (as yet )nameless from norway.
I meant the thyroid testing bit was his as Lyn out in site
that was a fascinating read. I was very fortunate to have been diagnosed in 1963 with pendreds syndrome due to a large goitre and hearing loss. I would hqve been institutionalised as a ‘cretin’ (as I’m sure a few other less fortunate people were) had our GP not happened to have attended a lecture - probably by that professor. Was then a 4 yr old guinea pig in and out of Middlesex hospital until 16 yrs old. I don’t remember having blood tests at all and screamed the walls down just having X-rays to check bone growth as it was suboptimal. How did they test blood levels? All I know is that I ended up in my late teens on a dose of 300mcg daily for 20yrs - way above todays limits. No GP tested it til I was 32yrs old and am paying the price now methinks with my heart, cancer burden etc. but better then being institutionalised. So now I know so much more about Ft3/4 testing - thank you.
Hi there - wow what a story and thanks for telling me/us about your journey. I am not so sure that your heart issues are anything to do with the high doses you were put on for those 20 years - if you had been suffering with palpitations/sweating profusely or even being hyper just generally energy wise then I would say you were on too much.
It is a fallacy in my opinion what the 'professionals' say about heart damage if you are on too much thyroid hormone - it is the opposite that is true - not enough then the heart can suffer as the metabolic rate drops down and then as the heart is a muscle it will become baggy etc. - my Mother was in heart failure not diagnosed with hypothyroidism until 82 years of age and given thyroxine and her enlarged heart went back to normal size. Obviously if you were suffering with the symptoms mentioned then I would yes you need to drop down the medication but if not then your body is needing it.
Years ago before the blood test - probably before 1963 - they diagnosed hypoT by symptoms only - some of which I am going to post shortly under a diagnosis type post - and there was no T3 needed because patients were put on 200 mcg in those days which automatically converted nicely to enough T3 - it is because we are being put on so little a dose that there are problems for some of us as the amount of T4 given is not enough to give us the correct amount of active hormone T3.
May I ask did your heart issues occur when they dropped your dosage down to the lower figure ? Be interesting to know. Thanks for your post it has helped me understand a little more about this incredible gland and how it is virtually being abused by the medical profession who know so little how to keep it happy !
Heart health and the thyroid - this is a good article -
Interesting article. You can see where the reliance from GPs here on just testing TSH comes from. We know this is wrong, but when they were trained, they were taught this was the gold standard. When you are trained on a "fact" it is difficult to dismiss it.
Around 200 million people worldwide have been diagnosed with thyroid disease. With these numbers, you would think the medical staff would be trained to spot and treat effectively, move with the times, but having seen a young GP, the TSH "fact" has been implanted recently. So we all have to fight our own individual battles when we are ill.
Thank goodness for this forum!
You would think that certain people at the top of the tree would see how many people are unhappy with their treatment and perhaps listen to Professor Toft - poor man was on the panel who decided on the criteria for the blood test ratios and he has now admitted he got it wrong but is unable to get anyone to listen to him as it suits them to say your blood tests are fine - I suffered with this issue for 15 years and nearly died until being forced to go to Belgium to get help. I did in fact write to the Professor telling him my story which was not pleasant - I was sub clinical with over 100 serious symptoms that were at times life threatening. My career as well as my health was ruined - I somehow think he took the hint.
What I can tell you - a certain endocrinologist in a large London Hospital no names mentioned is a trainer and is training his new endo's not to extend their knowledge into T3 hormone application for patients but to tell them it is not necessary at all. Well actually Professor Toft says that in his video - years ago 200 mcg was given to thyroid patients which automatically concerted to enough T3 to satisfy our bodies - I doubt very much if this trainer is advocating those high doses so nothing will change I daresay.
Here are papers etc. on the subject by Professor T.
BMC Endocr Disord
2019 Apr 18;19(1):37.
doi: 10.1186/s12902-019-0365-4.
Time for a reassessment of the treatment of hypothyroidism
• PMCID: PMC6471951
• DOI: 10.1186/s12902-019-0365-4
Cite
Abstract
Background: In the treatment for hypothyroidism, a historically symptom-orientated approach has given way to reliance on a single biochemical parameter, thyroid stimulating hormone (TSH).
Main body: The historical developments and motivation leading to that decision and its potential implications are explored from pathophysiological, clinical and statistical viewpoints. An increasing frequency of hypothyroid-like complaints is noted in patients in the wake of this directional shift, together with relaxation of treatment targets. Recent prospective and retrospective studies suggested a changing pattern in patient complaints associated with recent guideline-led low-dose policies. A resulting dramatic rise has ensued in patients, expressing in various ways dissatisfaction with the standard treatment. Contributing factors may include raised problem awareness, overlap of thyroid-related complaints with numerous non-specific symptoms, and apparent deficiencies in the diagnostic process itself. Assuming that maintaining TSH anywhere within its broad reference limits may achieve a satisfactory outcome is challenged. The interrelationship between TSH, free thyroxine (FT4) and free triiodothyronine (FT3) is patient specific and highly individual. Population-based statistical analysis is therefore subject to amalgamation problems (Simpson's paradox, collider stratification bias). This invalidates group-averaged and range-bound approaches, rather demanding a subject-related statistical approach. Randomised clinical trial (RCT) outcomes may be equally distorted by intra-class clustering. Analytical distinction between an averaged versus typical outcome becomes clinically relevant, because doctors and patients are more interested in the latter. It follows that population-based diagnostic cut-offs for TSH may not be an appropriate treatment target. Studies relating TSH and thyroid hormone concentrations to adverse effects such as osteoporosis and atrial fibrillation invite similar caveats, as measuring TSH within the euthyroid range cannot substitute for FT4 and FT3 concentrations in the risk assessment. Direct markers of thyroid tissue effects and thyroid-specific quality of life instruments are required, but need methodological improvement.
Conclusion: It appears that we are witnessing a consequential historic shift in the treatment of thyroid disease, driven by over-reliance on a single laboratory parameter TSH. The focus on biochemistry rather than patient symptom relief should be re-assessed. A joint consideration together with a more personalized approach may be required to address the recent surge in patient complaint rates.
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