I struggle. I really do. With sentences like this:
As such, clinicians caring for these patients should listen to their concerns, validate their symptoms, and collaborate with them to form a management plan that includes the evaluation of thyroid and nonthyroidal disease (e.g., iron deficiency anemia, sleep disturbance in patients with fatigue) if persistent hypothyroid symptoms are present.
It doesn't seem too bad at all - until you hit "if persistent hypothyroid symptoms are present". We see so many here with low iron and try to support their addressing the issue. But why should iron deficiency anaemia be addressed in those with persistent hypothroid symptoms but not, it appears in anyone else?
And it serves to confuse as to whether the symptoms of iron deficiency are the same as those of hypothyroidism?
I too find this remark confusing. I am also told my symptoms of iron deficiency are because of the RA and absorption problems… How can one get help when a doctor “uses” another illness to explain other problems and there is never a solution. I understand that one health issue can trigger another health issue but we, patients, rarely seem to get the help we need. Do I expect too much from my doctor/consultants?
How is that so many patients showed a clear preference for combination therapy yet they claim there was no difference in outcome, that IS a difference in outcome in my opinion - it’s just a load if old nonsense trying to disprove what is blindingly obvious to anyone with half a brain , namely the closer the treatment to the original thing the thyroid made the better the outcome will be. How can they be so blindingly stupid? They don’t even understand how it actually works but are happy to use just one hormone and claim it’s perfect.
To me, the basic problem is that the medics almost always approach thngs from a statistical viewpoint - ie they compare the patient against that viewpoint. Virtually none can get away from patient diagnosis by statistics -they don't seem capable of the necessary change to patient appraisal first. It is to me amazing that they simply do not see the fallacy, and nothing and no one will move them.
Well said!! Randomly assigning people to treatment groups could well be enough to iron out differences, as they are not giving each person the treatment that THEY need. Some people will be getting be getting a treatment that suits them, while others won’t.
I am pleased the review and the earlier study were published, it's a step in the right direction towards acceptance that some people do still have unresolved hypo symptoms on Levo for physical rather than psychological reasons. and towards better designed trails being done.
But still this is a problem ....
"a trial of combination therapy that include T3 (dosed in a physiologic ratio to L-T4) might be considered.." That's OK , but who's physiological ratio are we talking about ....yours, mine, or uncle tom cobbley's
I think this is a bit of a red herring and confuses the situation. Firstly, targetting the serum ratio whatever it is makes no sense. Levothyroxine and liothyronine have different pharmacokinetics, different absorption rates and half-lives. The ratio you put in your gob is not the ratio that ends up in the blood. Nonetheless, whatever the ratio it is easy to titrate the doses such that you restore typical serum fT3, fT4 levels and ratios. This has been done many times and doesn't work for most of the patients who need T3 to avoid profound symptoms. Putting T3 into the blood is not the same as T3 converted from T4 within cells that then finds its way into the blood. If deiodinase is impaired the problem is deeper than simply restoring serum T3.
The point i was trying (but forgot ) to make, was that they need to not be so fixed on the idea of any particular ratio being the right one... since we are all clearly so different in this respect before we go wrong ... so trials need to allow (somehow )for finding the right mix that works for the individual .
I agree. The evidence I see from my own experience and observation of posts on the forum is that most often people need a level of T3 well beyond their normal T3 / T4 ratio. i.e. their condition is such that restoring normal serum T3 levels is not sufficient. I'm concerned that by getting into technical details about what natural ratios are we will divert attention away from the real requirements. I certainly agree that we need to get the right mix for each individual.
(I don't like T3 : T4 ratios because they change so much in each person. The body seems to try to keep stable T3 levels and this results in varying ratios as T4 goes up and down.)
The authors of this commentary are no doubt well intentioned but like many of their colleagues lack a grounding in basic scientific principles. There is an assumption that patients will recover when TSH is normalised – they dictate that experimental data should conform to their hypothesis. Science works the other way around.
“These findings support the need for large RCTs that are adequately powered and designed to answer the clinical question of which patients with hypothyroidism, if any, benefit from combination therapy.” The assumption underlying this pseudo-scientific statement is that such patients are not easily identified, and their morbidity is so minor that only a large scale RCT will reveal subtle symptoms. Such patients are banging on their doors daily with life destroying symptoms. An appropriate small-scale study is adequate.
Elementary investigations have not been carried out. For example, grab a few dozen such patients and analyse their TFTs. Is their TSH appropriately elevated compared to fT3, fT4? Once a cohort is identified establish what doses of T3, T4 are needed to resolve their symptoms. My experience and observations of forums posts is that many patients need L-T3 doses of around 40 mcg daily.
There is a diktat that all patients may only recover with a normal TSH. TSH regulation is controlled by feedback from fT3 and fT4 and feedforward by TRH. TRH feedforward is crucial, it not only controls how much TSH is produced but also its bioactivity, if TRH is insufficient there is less TSH and this TSH is less active.
We need to bear in mind TSH stimulates both thyroidal secretion and T4 to T3 conversion, in particular type-2 deiodinase (D2) which regulates local T3 levels in tissues such as the brain and skeletal muscles. If a patient’s TSH is not responding adequately to low normal fT3, fT4 there will be impaired deiodinase. Giving such patients thyroid hormone will push TSH lower, further reducing the rate of T4 to T3 conversion. This leads to local tissue hypothyroidism, restoring serum T3 with a little L-T3 will not restore local T3.
The Pollock study ncbi.nlm.nih.gov/pmc/articl... was a response to Dr Skinner’s call for a trial of levothyroxine in patients with signs and symptoms of hypothyroidism and normal TFTs. Like the studies that followed it this study found no benefit in levothyroxine therapy. When given levothyroxine the small control group had a highly significant (p=0.002) increase in fT3, there was no such response in the patient group. The evidence is that some patients fail to convert supplementary L-T4 to T3. If patients have impaired D2 activity it’s no good just restoring serum T3, tissues dependent upon D2 will still be hypothyroid.
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