55 year old male, Have been taking Levothyroxine for 10 years when first diagnosed with Hypothyroidism. My current dosage is 75mcg and 100 mcg on alternate days. I have most of the usual hypothyroid symptoms such as general fatigue, sore muscles and cramps, weight gain and low moods. My most recent lab results are below. I’ve read on this site that I should maintain optimal levels of ferritin, folate, B12 and vitamin D. I’ve never had these tested, but will ask for this to be done when I’m next tested.
TSH 1.34 miu/L (0.38-5.33)
Free T4 8.7 pmol/L (8.0-17.00)
Free T3 5.5 pmol/L (3.8-6.0)
I’ve learnt that ideally my TSH should be below 1.0, which mine is not, so wonder if I should have my Levothyroxine dosage increased? My FT4 is at just 51% of its range, so this also supports the proposed increased dosage. However, I can see that my FT3 is at 92% of its range and I’ve read numerous times that the FT3 reading is the most important. If this is true, how can my FT3 be so "good" when I'm experiencing debilitating symptoms?
My FT4 to FT3 conversion ratio is 1 to 1.6 (I’ve learnt from this site that the expected range on T4 meds only is 1 to 3.5-4.5) Mine is very low. Does this mean I’m converting FT4 to FT3 really well? Why am I so far out of the expected range?
As I’m new to learning about Hypothyroidism, I would be grateful for any suggestions as to what I should do to rid myself of hypo symptoms. My GP has referred me to see an Endo next week, so any help re how I can get the most from this appointment would be great.
Thanking you in advance.
Written by
Ogbourne
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Recommended that all thyroid blood tests early morning, ideally just before 9am, only drink water between waking and test and last dose levothyroxine 24 hours before test
This gives highest TSH, lowest FT4 and most consistent results. (Patient to patient tip)
Is this how you tested
Are you sure you have results written correctly?
FT4: 8.7 pmol/l (Range 8 - 17)
Ft4 only 7.78% through range
FT3: 5.5 pmol/l (Range 3.8 - 6)
Ft3 at 77.27% through range
List of private testing options and money off codes
Even if we frequently start on only 50mcg, most people need to increase levothyroxine dose slowly upwards in 25mcg steps (retesting 6-8 weeks after each increase) until eventually on, or near full replacement dose
Consider starting levothyroxine at a dosage of 1.6 micrograms per kilogram of body weight per day (rounded to the nearest 25 micrograms) for adults under 65 with primary hypothyroidism and no history of cardiovascular disease.
In the majority of patients 50-100 μg thyroxine can be used as the starting dose. Alterations in dose are achieved by using 25-50 μg increments and adequacy of the new dose can be confirmed by repeat measurement of TSH after 2-3 months.
The majority of patients will be clinically euthyroid with a ‘normal’ TSH and having thyroxine replacement in the range 75-150 μg/day (1.6ug/Kg on average).
The recommended approach is to titrate thyroxine therapy against the TSH concentration whilst assessing clinical well-being. The target is a serum TSH within the reference range.
……The primary target of thyroxine replacement therapy is to make the patient feel well and to achieve a serum TSH that is within the reference range. The corresponding FT4 will be within or slightly above its reference range.
The minimum period to achieve stable concentrations after a change in dose of thyroxine is two months and thyroid function tests should not normally be requested before this period has elapsed.
Request/insist on 25mcg dose increase in levothyroxine
Retest in 6-8 weeks
Likely to need further increases in dose over coming months
Guidelines suggest eventual dose …..
90kg x 1.6mcg Levo = 144mcg Levo per day
you might need a bit less …or you might need a bit more
When on correct dose of just levothyroxine most people will need Ft4 at least 70% through range
Clearly your Ft4 is currently far, far too low because you are not on high enough dose levothyroxine
Also request GP test vitamin D, folate, B12 and ferritin levels
Vast majority of endocrinologists are diabetes specialists and useless for thyroid
When FT4 is low the body initially raises FT3 in an effort to maintain wellbeing but this will be at the detriment of other hormones and is not sustainable. You need a slow Levothroxine dose increase that will raise T4 levels and eventually reduce T3, as hormonal enzymic activity normalises.
Thank you for the link to the calculator. Yes I had made an error with my initial calculations, I mistakenly thought it was a simple % calculation of the max range compared to my level.
I'm very interested in what you wrote re body raising FT3 when FT4 is low, but this is at the detriment of other hormones. Please can you expand on this a little?
I too was puzzled by 'raising FT3 when FT4 is low' so I googled thyroxine metabolism.
Short version: It's correct
Long version: In that search I found an article by Yan-Yun Liu which states that deiodinase type 2 (which every schoolboy knows converts T4 to T3 and produces most of our T3 apparently) levels are inversely related to serum T4 levels. In other words as T4 falls the body tries to make more T3.
A bit like being nearly out of petrol so going faster before the tank runs out.
In all that searching I discovered Selenium. Wow is that one important element?
Most T3 in the brain is locally produced by DIO2 but equally DI01 is just as important for peripheral conversation in the body and its role in RT3 clearance that paves the way for further T3 to be converted by both enzymes.
All DI01, DI02, & DI03 are not only influenced by each other but thyroid hormone levels and other environmental factors and health conditions. Equally they may play a part in locally modifying thyroid hormone bioactivity independent of serum thyroid hormone levels. As said to Ogbourne, read Tania Smith blogs at Thyroid Patient Canada for great information clearly explained on what is an extremely complex topic ... . thyroidpatients.ca
Yes, iodine and selenium are the two trace elements that the production and metabolism of thyroid hormone is most dependant upon.
If different deiodinases are responsible for conversion in different tissue sites, can we use the mutations on different deiodinase genes to explain why some get X thyroid symptoms and others get Y.
Eg. Person A gets depression and weight gain but doesn’t get tired or constipated, Person B gets tired and constipated but doesn’t get depressed or gain weight.
Can these differences be accounted for by different DIO mutations? Or is that ridiculously simplistic?
Absolutely correct ✅✨because it's how that impairment interacts with other genes that may carry it or magnify its inadequacies.
The scientists and professors give us the gist but we are all different and there is no formula to fit all. Even having an DI02 mutation is only an indication of impairment but doesn't guarantee or give depth of impairment.
Some are 'lucky' and don't need to be so astute regarding life style choices but with evolution and all todays surrounding chemicals, plastics, etc, many of us will only last in any acceptable fashion 😁 with mindful life style choices. Hence the gluten free arising, etc.
I’m not doing Zoe, but I’ve been following with interest the reports of Regenallotment et al. I’ve done more stool tests than I like to admit, and I’ve had an FMT so I’d certainly be interested. My torrid love affair with keto left me feeling angry and frustrated with food, but I know it deserves more dedication and precision than I currently give it.
I’m elbow deep in suprachiasmatic nucleus these days - it’s my new cortisol - the light diet 💡
Genetics is very interesting Radd, because I have been told by multiple practitioners I have quite beautiful genes - no MTHFR and relatively few other problematic ones, a bit of a SOD issue but nothing much more to write home about. Yet I’ve diagnoses, symptoms galore! Epigenetics is a lever I must pull on a bit harder I think.
As my major symptoms have always been mental/cognitive, I can tend to binary thinking “I’ll sit back and wait for the meds to work while I eat these coco pops” kind of thinking OR “I’ll just eat meat for 18 months and wait to get better that way.” But I am coming around to the idea of sensitizing mechanisms, creating a cohesive environment between my systems, appreciating the psychological connection to health… it must all give these meds their best chance at helping me…
The effects are on multiple levels such as the TSH that will boost T4-T3 conversion when elevated before medicating thyroid hormone replacement meds, and also improved T3 synthesis in the gland dictated by how much residual thyroid tissue remains.
You are medicating and an FT3 at 77.27% will mean something very different to your body if the FT4 is at 7.78% rather than say 60% through reference range. You are at present converting too well due to up-regulated deiodinase activity, and most likely won’t need that much more thyroxine as achieving the correct T4:T3 ratio by highering T4 a little and dropping T3 a little will further boost better deiodinase behaviours.
This is in opposition to taking T4 levels too high when something called ubiquitination refers to the best biological limit on how much T3 can be converted, as once exceeding your individual sweet spot (ratio), convertion will start to decrease and unused T4 can start working against you in the form of inactive metabolites that become destructive when in excess. It is an extremely fine balance.
All hormones work together as are influenced by one another in complex feed back loops influenced by factors such as genetic impairments, other health conditions and lifestyle. On this forum the adrenals are known to compensate for inadequate thyroid hormone and low levels of cortisol and DHEA are incredibly common. The problem is not usually with the adrenals themselves but an induced dysregulation within the HPA axis that with time becomes a new baseline, and simply will not allow enough hormone to be made until thyroid hormones have been optimised for quite some time. In the interim further negativities/conditions may be acquired and all issues further compounded upon introduction of Levothyroxine that increases metabolism widening gaps further.
Equally sex hormones suffer with long term undiagnoised hypothyodism, and all hormones are further negatively influenced (even if indirectly) by the chronic inflammation that usually accompanies thyroid autoimmune disease.
ps - You won’t get this knowledge from many endos and it’s worth educating yourself. A great site to start is the Thyroid Patients Canada blogs written by Tania Smith from which I have learnt much of my knowledge. thyroidpatients.ca
I agree you need an increase in levothyroxine. This is usually done in 25mcg increases, then re tested 6-8weeka later, though your GP will insist on 2-3months I'm afraid. Ideally TSH, FT4 & Ft3 though on the NHS it will be TSH and maybe Ft4. You can do private tests reasonably priced look on Thyroid UK.
one possible reason for relatively high fT3 is that when the thyroid is failing, and the low fT4 T level causes the TSH to go high , the thyroid responds by increasing the ratio of T3 to T4 that it makes. ... it appears to be a kind of safety net. ie. 'make sure plenty of ready made, instantly useable T3 is available, as there may not be much T4 knocking around to convert when needed" .. kinda thing.
This pattern of abysmally low low T4 and relative good looking T3 is often seen at diagnosis (before levo is given and lowers the TSH again) , but i wouldn't have thought your TSH is currently high enough to be triggering this effect , so i don't know if it explains why your fT3 is so high relative to T4 or not .
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