This is interesting in that it combines T4 monoterapy and carbohydrate response. could be a clue as to why patients on T4 only can have difficulty losing weight.
Agnieszka Kozac, Gilmara Gomes de Assis, Urszula Sanocka, Andrzej Wojciech Ziemba
Hypothyroidism is associated with a lower metabolic rate, impaired glucose tolerance, and increased respon-siveness of sympathetic nervous system to glucose ingestion. The Levothyroxine (LT4) monotherapy is the standardtreatment for hypothyroidism; however to what extent this treatment restores the patientmetabolism has not been verified.The aim of this study was to test the hypothesis that standard LT4 therapy may not restore proper metabolic response to carbohydrate ingestion.
Conclusion
Standard T4-only treatment for hypothyroidism does not restore the normal metabolic reaction to carbohydrate which is observed in healthy people.
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I would agree with that as it fits with my own experience. Is there a solution though, or is it just 'watch the carbs'? I imagine the majority of hypo patients are on T4 treatment.
Makes sense. Just had a similar conversation this morning with my enlightened physio. He called it ‘carb tolerance’; reckoning it interferes with T4 to T3 conversion and until this ‘tolerance’ is dealt with (ref:Lulu2607) conversion will continue to be poor. Hence perhaps the good reaction many people report from introducing T3 into their equation - if only some of us could at least try it.
So as far as I can make out, the question is, what’s in natural thyroxine other than T4 and T3 that is so necessary for the metabolism of carbohydrates? And is anyone finding out? And can they hurry up!
It's now agreed that, in T4 mono therapy, a given dose of T4 doesn't produce as much T3 for the same T4 level. It won't be theT4 that is given, but the relative failure to produce enough T3 from it for weight control purposes
I think T2 is supposed to be involved in metabolism, but not sure if it affects carbohydrates I think it has an action on mitochondria & it does seem to aid weight loss. One would get more of it if taking T3 or NDT There is some research been done on it.
As I understood it, although the hypothyroid subjects were only on T4, they did measure FT3 levels, and on page 21 they referred to lack of RMR increases despite increasing FT3 levels. One of the explanations of the lower metabolic rate they put forward was “..deficiencies in other than triiodothyronine and thyroxine active substances secreted by the thyroid gland and/or THs-active intermediate metabolites. Some of the active substances from thyroid gland are present in desiccated thyroid extract, which may be one of the explanations of increased satisfaction with the therapy of patients taking desiccated thyroid extract than patients taking LT4..” I took it to mean there were substances in desiccated thyroid extract other than T4 and T3 that were at work.
I thought it was very interesting what they said on page 17 about higher plasma sodium levels in the hypothyroid patients at all time points. I wake up feeling very dehydrated every morning.
"While lower RMR is a characteristic of hypothyroid state, patients undergoing treatment should demonstrate normalized RMR levels. Such normalization was reported by Wolf et al. (1996), however, TSH-suppressive doses were used for this [39]. Although, lack of RMR increases despite increasing plasma fT3 level, was also reported [22]. The normalized TH blood concentration with slower RMR suggests a state of “tissue hypothyreosis condition” characterized by a difference between plasma THs and THs concentration and/or activity inside cells which is assumable when considering the complexity of mechanisms governing the proper tissue response to TH stimulation [40, 41]. Such phenomenon has already been observed in NA dynamics in non-treated hypothyroid subjects [42]. Other possible explanation of lower RMR can be resulting from deficiencies in other than triiodothyronine and thyroxine active substances secreted by the thyroid gland and/or THs-active intermediate metabolites........"
This suggests that with higher Levo doses (TSH-suppressive doses ) ~ ? and therefore potentially higher fT3 levels on levo ? ~ RMR can be restored for some people , as long as Levo dose is high enough .
The reference to a report of "lack of RMR increases despite increasing plasma fT3 levels" is a finding from a different study (ref 22).... but unfortunately there is no easy access to any of the data from that one , just a brief abstract which doesn't mention the fT3 findings, so it's difficult to know the strength of the evidence which led them to this conclusion .
The study that is the subject of this post doesn't give us any fT4 /fT3 data, and they don't mention any of their own observations about fT3 levels from this study .
So i think it's still possible that improving an individual's fT3 level ( by any source, including higher doses of levo and or /adding synthetic T3) would be able to improve the RMR ?
In the study they used resting metabolic rate as a measure, as it reflects what your metabolism is doing, including thermogenesis, eating, digesting and processing food.
Interesting. I've followed a low carb diet for years, as it's the only thing that really works for me.
When I first got diagnosed, I put lots of weight on, and also stopped low carving for a while as I felt so terrible.
Was on levo, and started back on low carb diet, and it just didn't work at all. It's only when I started adding T3 medication in that the diet started working again, and I lost the 4 stone I had put on.
This available paper links low carbohdrate diet and Hashimoto's disease
Drug Des Devel Ther. 2016; 10: 2939–2946.
Published online 2016 Sep 14. doi: 10.2147/DDDT.S106440
PMCID: PMC5028075
PMID: 27695291
Effects of low-carbohydrate diet therapy in overweight subjects with autoimmune thyroiditis: possible synergism with ChREBP
Teresa Esposito, Jean Marc Lobaccaro, Maria Grazia Esposito, Vincenzo Monda, Antonietta Messina, Giuseppe Paolisso, Bruno Varriale, Marcellino Monda, and Giovanni Messina
In the paragraph in red it states “Thyroid hormone may increase symptoms of diabetes mellitus, diabetes insipidus, or adrenal insufficiency. Adjustment of treatment measures for these endocrinological diseases is necessary if thyroid hormone therapy is added.”
Any idea to what “symptoms of diabetes Mellitus” means?
It’s quite an unusual phrasing so I’m not sure if it means increases/decreases insulin/carb sensitivity, increases or decreases hypoglycaemic or hyperglycaemic events… or what? 🤔🤔🤔
I couldn’t see the relationship between diabetes symptoms and Thyroid hormone, as normally it’s quite the opposite with thyroid function improving blood sugars can improve too.
But don’t worry, I was just curious if you knew, maybe someone will stumble on our exchange 😬😬
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Optimizing the treatment of hypothyroidism
why does t3 decrease t4 levels and can this effect symptoms. 
Why aren't All Doctors Restoring Hormones to Optimal Levels and/or Effects?
