Hashihouseman in reply to Clutter6 years ago

Are you saying learned and experienced endocrinologists views are invalid? Everything in the range of the debate is valid for consideration unless it is factually absurd and or lacking in sufficient evidence or theoretical possibility to even warrant further investigation.

A substantial body of recent research points to individual set points of thyroid homeostasis being defined by at least free T3, free T4 and TSH. Lab normal ranges of individual hormone levels are not necessarily the yardstick for optimal hormone replacement. Steady state, sustainable, reasonably risk and symptom free managed thyroid homeostasis is the holy grail of replacement therapy and the statement 'The appropriate dose of levothyroxine is that which restores euthyroidism and serum TSH to the lower part of the reference range - 0.2-0.5mU/l.' is possibly over simplistic and over generalised.

Sticking to the paradigm that patients should expect that Levothyroxine replacement therapy will morph euthyroid blood levels into different part, of the Lab ranges and thereby define appropriate treatment ignores all the people who do this and still feel unwell or suffer side effects. It also ignores the possibility that empirical euthyroid blood levels are a valid target for replacement therapy . Achieving these levels with Levothyroxine alone may indeed be unrealistic - hence the debate on more subtle combination replacement therapies.....

It often seems prescribers are overly reliant on ramping up Levothyroxine doses to meet patient frustration about symptoms and end up with unecessariIy and perhaps unhealthily low TSH and unecessarily high free T4 to pump up free T3. Some individuals may have genetically lower or higher set points for T3 which were never known before they became athyreotic. It may be reasonable to suggest there is no such thing as 'unequivocally normal' T3.

It may be that some of the frustrations of treatment come from excessive free T4 and overly suppressed TSH. And then there are the considerations of valid opinions based on valid research that suppressed TSH can have long term health risks:

Dr Graham Leese, from Ninewells Hospital and Medical School, led a research team examining patients on thyroxine replacement therapy. They studied how variations in these patients’ TSH levels affected their long-term health. The study followed 16,426 patients taking thyroxine (86% female, mean age 60 years) and examined how their risk of contracting a range of diseases varied with their TSH levels.

The study found that patients with very high (>4.0mU/l) or suppressed (≤0.03mU/l) TSH levels more frequently suffered from heart disease, abnormal heartbeat patterns and bone fractures compared to patients whose TSH levels are in the normal range (0.4-4.0 mU/l). Patients who had a slightly low TSH level (0.04-0.4mU/l) did not have an increased risk of contracting any of these conditions.

Clutter in reply to Hashihouseman6 years ago

Hashihouseman,

Are you saying Dr. Toft, consultant endocrinologist and ex-president of the BTA views are simplistic?

I'm saying some endocrinologists are neither learned nor experienced re thyroid. Amongst them I include those who think TSH is the gold standard by which thyroid levels are judged and that FT4 and FT3 are unnecessary; those who dose solely by TSH levels; those who think FT3 levels below range are unimportant; those who do not accept that Levothyroxine can cause adverse symptoms; those who say Liothyronine is a placebo, those who tell patients on Levothyroxine that their symptoms are psychological and nothing to do with thyroid when the patient's TSH is >6 and they are clearly undermedicated; endocrinologists who claim a patient was never hypothyroid at diagnosis without seeing their thyroid levels at diagnosis and take them off replacement, discharge them, and then GP has to re-refer when TSH rises, etc. etc.

I have read research re suppressed TSH causing AF and osteoporosis with interest. The Rotterdam Study finds no association between TSH and atrial fibrillation and a meta-analysis of fractures in patients with TSH <0.1 found one extra hip fracture per 1,000 patient-years.

My TSH has been suppressed <0.01 post thyCa. Endo would like it less suppressed at 0.05. Three dose reductions didn't budge TSH but FT4 and FT3 dropped considerably so it seems likely my TSH set point has been reset. I declined further dose reductions in favour of feeling well today as opposed to increased risks of adverse health in the future.

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Hashihouseman in reply to Clutter6 years ago

I was saying that statement you referred to may be over simplistic and over generalized, and there’s evidence to suggest that; I don’t know enough of dr Toft to have formed such a sweeping opinion about all his views;). And I agree with all of your views expressed in your second paragraph, I’m no fan of any of the half dozen nhs and private specialist endocrinologists I have seen or of the reports and opinions promulgated from others. Having said that I don’t write them all off and as I said in my previous reply, regard all views as valid for consideration in the discussion unless they are obviously ill founded lacking in evidence or lacking basic theoretical consistency with thoroughly established understandings.

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HLAB35 in reply to Clutter6 years ago

Thanks, that's fine.... the results just seemed a little 'off'. I just wasn't sure whether it was autoimmune.

Clutter in reply to HLAB356 years ago

HLAB35,

If antibodies were high when Hippyhappy234 was diagnosed then it is autoimmune (Hashimoto's). If not, then it's not Hashimoto's which caused hypothyroidism.

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