Be interested in comments. I've given it a quick scan but it needs more than that!
Hypothyroidism: The difficulty in attributing symptoms to their underlying cause
Common symptoms of overt hypothyroidism are non-specific and include fatigue, lethargy, and dry skin. Although the diagnosis is considered to be straightforward, no single symptom can be used to identify patients with overt hypothyroidism, while many patients with subclinical hypothyroidism are asymptomatic. A large population-based study on the spectrum of symptoms in subclinical hypothyroidism showed similar rates of thyroid disease-related symptoms compared with euthyroid subjects, while the TSH concentration had no impact on symptom score. Together, these findings make it challenging to attribute symptoms to their underlying cause. This is also true in the case of unexplained persistent symptoms in levothyroxine-treated patients. Although generally considered a life-long replacement therapy, successful thyroid hormone discontinuation resulting in euthyroidism has been reported in approximately one third of patients. Thus, we overtreat patients with (subclinical) hypothyroidism, highlighting the importance of reliable diagnostic criteria. The diagnostic process, including the implementation of robust TSH and FT4 reference intervals, is especially challenging in specific situations including aging, pregnancy, non-thyroidal illness, and central hypothyroidism. There is a clear need for improved adherence to current guidelines from scientific societies and for willingness to manage symptoms without a clear pathological correlate, especially in the case of mild TSH elevations. This review will highlight recent literature on this topic and offers some practice points.
"Although generally considered a life-long replacement therapy, successful thyroid hormone discontinuation resulting in euthyroidism has been reported in approximately one third of patients."I’d love to see a citation for this.
Clinical Outcomes After Discontinuation of Thyroid Hormone Replacement: A Systematic Review and Meta-Analysis
Conclusions: Low-quality evidence suggests that up to a third of patients remained euthyroid after thyroid hormone discontinuation, with a higher proportion of patients with an initial diagnosis of SCH remaining euthyroid than patients with an initial diagnosis of OH. A deprescribing framework focusing on adequate selection of patients for deprescribing LT4 and a systematic process is warranted to guide clinicians in re-evaluating the need for LT4 in their patients.
Thank you so much! Astonishing how they’ve taken this shoddy “evidence” and twisted it so… No wonder so many are undiagnosed/improperly treated if this is how they construct their research premises.
Reviews can be useful in drawing attention to things that are otherwise likely to be missed or ignored. And collect things that would take an unfeasible time for each person to find for themselves.
But when a review mis-leads its readers (even if inadvertently), it becomes yet another barrier.
Exactly. They seem to pick and choose what shows things that they want to show. It looks like very shaky evidence indeed.
As someone who stopped Levo for a few weeks and ended up with a TSH of 240 with symptoms to match, then struggled to restart Levo, wild horses would never make me repeat that.
It's irresponsible to even think about stopping someone's thyroid replacement in my book. It's not like you can be back on track in a couple of weeks.
Although generally considered a life-long replacement therapy, successful thyroid hormone discontinuation resulting in euthyroidism has been reported in approximately one third of patients.
Is 'euthyroidism' here what my GP seems to think I wonder?
It goes something like: Your TSH is 4.8 and your T4 is 13.
Yay, euthyroid equilibrium achieved!
What are they saying counts as euthyroid status?
I'm confused and I can't wholly make sense of it - not taking meds
I realise it is ridiculously cumbersome, but when we see the word "euthyroid", we should see a qualification. Imagine "euthyroid" (NICE 2019) - meaning "euthyroid as defined by NICE in 2019". Or some other convention which directly links the actual use of the word with one of its formal definitions.
"Another pitfall that should be acknowledged is that not all groups benefit from using the same TSH and FT4 reference intervals. Clinical studies in euthyroid patients using L-T4 showed that FT4 concentrations in this group are significantly higher, and more often above the upper reference interval, than in non L-T4 treated people (32, 48, 49) indicating that in this group a higher upper reference limit may apply. In addition, FT3 concentrations and FT3/FT4 ratios are lower in this group compared to non-L-T4 users, a finding probably more outspoken in athyreotic patients due to the absence of any endogenous T3 production. Therefore, the question is justified whether the current reference intervals suffice for persons using L-T4. As mentioned previously, Salas & Bianco (38) suggested that (F)T3 concentrations may reflect TH status in L-T4 treated people even better than FT4. On the other hand, an analysis of the relationship between psychological well-being and FT4, FT3 and TSH in a large group of patients on L-T4 showed that psychological well-being correlates with FT4 but not with FT3 levels (50). Thus, optimal biochemical monitoring during TH treatment is still a matter of debate and pitfalls regarding the measurement and interpretation of TSH and FT4 should be acknowledged and taken into account by laboratory specialists and clinicians."
"In our opinion, subclinical hypothyroidism and its treatment in older adults should probably be a matter of personalized medicine and shared decision making. "
In MY opinion.. that should apply to treating subclinical hypothyroidism in ... everyone ...( like wot all Doctors used to have to do, before they had tickbox guidelines to follow .
Central hypothyroidism (CeH) is a rare form of hypothyroidism due to disturbances at the level of the hypothalamus or pituitary resulting in insufficient stimulation of the thyroid gland. The pathogenesis of CeH is variable and can be either congenital or acquired (e.g. iatrogenic, or by trauma, or autoimmunity)."
I like this bit which could be useful ammo for those needing to get central hypo considered by GP's :
"Since central control of the thyroid gland is lacking in CeH, TSH concentrations are low/normal and do not reflect TH status adequately in those patients. Therefore, FT4 concentrations are key in diagnosing and monitoring CeH. In most newborn screening programs for congenital hypothyroidism, TSH is measured as a first step. Since CeH is most often characterized by a low/normal TSH concentration, it can be challenging to detect CeH with this strategy. Furthermore, mild forms of CeH might even present with a FT4 concentration around the lower border of the reference interval and are therefore even more challenging to detect. Congenital CeH can be reliably detected in the newborn screening only if the protocol measures T4 as a first tier. While this is the case in The Netherlands and Japan, a TSH-based newborn screening is far more common and will not diagnose newborns with CeH."
pretty appalling that this admits to potentially missing central hypo in many babies for the cost of running an fT4 test alongside the TSH that is already done ,, what's the point of screening them all with a guthrie test if you don't do it properly ?
(in central hypo) ".. TSH cannot reliably be used to monitor L-T4 treatment efficacy and most information about TH status relies on FT4 determination. FT4 concentrations are influenced by the moment of L-T4 intake. Therefore, the European Thyroid Association (ETA) guideline on the diagnosis and management of CeH strongly advises to draw blood before or at least four hours after L-T4 intake (81) to allow reliable results. As previously discussed, FT4 concentrations are often higher in persons on L-T4, leading to the recommendation to pursue FT4 concentrations in the upper range of the reference interval in CeH. FT4 concentrations at the lower range of the reference interval in combination with hypothyroid symptoms indicate under-treatment. "
It seems to be rarer than it really is because they so rarely think about it as a possibility.
And only as difficult to diagnose as it is because they so rarely think about it as a possibility. Hence they don't look at the right things to diagnose it.
Autoimmune Pituitary Disease: New Concepts With Clinical Implications.
Anti-PIT-1 hypophysitis (anti-PIT-1 antibody syndrome) is a newly described pituitary autoimmune disease characterized by acquired and specific growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH) deficiencies.
This paper is one of a group entitled "(Re)defining Hypothyroidism: The Key to Patient-centered Treatment". It tries to get up-to-date, and at least addressing patient concerns, but all of it is still mired in statistical medicine - that is, in the range-OK; outside not. They simply cannot engage properly with the need to measure FT3 and why and when, I've written many times: thyroid paper writers simply cannot grasp the complexities of the physiology of control and how and what works where. I would say that evidence that only 1/3 of patients don't any longer need treatment is a bit shaky (I suppose this means subclinical hypothyroids) and once again it's statistics that seem to act as the guide and not the individual. It's true SCH is a really obscure situation and can be misunderstood. But if 1/3 patients can tolerate coming off T4 therapy, then 2/3 can't - the important majority. They are miles behind the proper understanding, but don't realise they don't really understand. Note the reply we made to the journalist for the Endocrinological Society recently. This emphasised the primary role of presentation over biochemistry. "Normal" TSH does not necessarily mean "euthyroid" and the ways in which patients present is wildly different and requires individual doctor and patient discussion first.
i can see they are 'trying' to improve ... but for the love of god ~ why are they all so thick ?.... we can all see so many bleeding obvious pitfalls in their thinking ......and we are the ones with the "so called" brain fog .
And very concerning that some will take that part of the paper as encouragement to try to get all of them off T4. Not just the 1/3. Seeing the 2/3 suffer, possibly seriously and for a long time. And only if they are lucky, stubborn and able to stand their ground being able to get back onto T4.
I'm thinking that the people who "get better" after suspension of meds might be people who are in the middle phase of Hashimoto/ autoimmune thyroid disease , where they've had a preliminary phase of HYPER with treatment by block and replace and then are in the mid phase begore the HYPO thyroidal phase predominates as the gland loses its ability to produce sufficient thyroxine . This is what happened to me with Anti tpo antibodies arriving the thyroid producing mechanism on the gland
without knowing whether the 'Euthyroid' TSH was really 'optimal' ie. 1 or 2 ish, with no symptoms , ( as opposed to 4 or 4.9999 ish and feeling like you're in freezer )
and without knowing whether EFFECTIVE /optimal treatment was given, as opposed to 'give em 25mcg and then say "no more cos your TSH is back in range" , (ie, take dose up enough for it to have a reasonable chance of improving symptoms while keeping T4 /T3 in range , and not being over panicky about TSH being a little lower than range as long as it want totally supressed )
Then you can't draw any conclusions AT ALL from studies saying "1 third of people were euthyroid when Levo was withdrawn "... especially if you never bothered to collect any data about how they actually felt.
Or how long they managed without meds? We have a good few descriptions on the forum of people feeling well (sometimes very well) for a period before finally crashing after stopping meds.
If anyone ever does define euthyroid for people who have already been treated for being hypo I would want it to be something like :
Come off Levo IF AND ONLY IF the patient has two tests three months apart which have TSH which is severely suppressed, and Free T4 and Free T3 which are both substantially above range.
If they can make people wait months and years to go on Levo then there should be an equivalent test for having it removed.
Alternatively, doctors could let the patient decide whether they wanted to risk coming off Levo, and the doctors should just leave patients to get on with it. That is a joke - it would never happen.
What is likely to happen though, if this ever became a big thing, is that doctors will decide whether the patient needs thyroid hormones. And if the patient wants them back they will probably have to meet the criteria for overt hypothyroidism again. But once TSH has been reduced by being on thyroid hormones there is no guarantee that TSH will ever go back to the heights of being officially hypothyroid again.
I have never had an official diagnosis of Central Hypothyroidism but I think I have it. My TSH has never reached 6, but it has been over range many times. I did come off my thyroid hormones twice, once in the first year and once in the second year, due to poor tolerance. Both times I felt as if I was galloping towards dementia at a huge rate of knots. I also struggled to get upstairs and had to crawl.
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