After appeasing an endocrinologist worried about my suppressed TSH by a cunning lab trick -- withholding NDT for three days before going for the blood work -- I realized I needed to titrate up the dose. Many thanks to those who replied with their NDT experience. I cranked it up to nearly double what I had been taking.
Then I gained intel about a fabulously brilliant endocrinologist at a competing health system to the one where I've been treated these past three years. I obtained a referral from my GP and saw the new endocrinologist a few weeks ago: a very clever woman who thinks outside the box. As I detailed the very long list of hypo symptoms, starting with weight gain and fatigue (and including ear wax so resistant to lavage that I had an appointment to have it scooped out by an otolaryngologist), she smiled knowingly and said, "What if it's something else? I see growth hormone deficiencies after traumatic brain injuries all the time."
The Insulin Tolerance Test is the gold standard for testing pituitary function, but here in the States, particularly for the elderly, they prefer the Glucagon-Arginine pituitary challenge, a six-hour endurance test monitored by a nurse at an infusion center. Clinical guidelines say it is not recommended unless there is compelling evidence that the results will be positive. With my history of TBI, the new endocrinologist was certain. (The other endocrinologists had been incurious, unconcerned, uncaring, except about my suppressed TSH)
It was an exhausting ordeal, and all I did was sprawl in a lounge chair from 8:30 to 2:30 and offer a couple of vials of blood every 30 minutes.
It seems that we need human growth hormone, (emitted by the pituitary in pulses, in response to demand detected by said pituitary), in order for peripheral conversion of T4 to T3 to take place. We can have plenty of free T4 floating around, but if there isn't enough GH present, nothing beneficial happens in the cells. Also, in a hypothyroid state, we have less GH stored in the pituitary to release and facilitate T4 to T3 peripheral conversion.
The results of the GH test came back after a few days. My pituitary performed like Erling Haaland, and the note back from the endocrinologist sounded somewhat accusatory: "The cutoff for growth hormone deficiency is 10 μg/l and you produced 25."
Good for me, but I'm anemic and do not have iron deficiency. The full iron panel came out middle of range in all the measures. The endocrinologist is passing me off to a hematologist, as though there's nothing else endocrine that could be producing the undesired effects.
It does seem plausible that a B2 deficiency could impair iron absorption and lead to anemia. They don't like to test for B vitamins here. But since riboflavin is water soluble, and since I had neglected to supplement B vitamins for several years, I've resumed the Jarrow B-Right. If I feel better and the anemia symptoms fade away, then I've solved it.
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I'm confused, are you saying this new endocrinologist was good or bad?GH has some effect on deiodinase but if this also affects deiodinase in the pituitary then lack of GH would tend to stop TSH going low. I don't know enough about it to understand whether the GH effect is only in peripheral tissues.
Certainly fT3 levels affect the brain and sleep. About 80% of GH is produced in derp stage four sleep. I find when my LT3 dose is about right I get derp sleep and awake rested with minor aches and pains resolved.
It does seem plausible that a B2 deficiency could impair iron absorption and lead to anemia.
Just to point out that B12 (yes, a different vitamin) deficiency does lead to anemia - even if you have plenty of iron. That is why B12 deficiency due to inability to produce Intrinsic Factor in your stomach is called PerniciousAnaemia.
In PA, anemia is often a later-stage sign. You can suffer many problems before reaching that point. Some never hit the criteria.
The cause of this Intrinsic Factor issue is autoimmune gastritis. And that can both reduce Intrinsic Factor AND stomach acid. The low stomach acid can lead to iron deficiency due to impaired digestion and absorption of iron.
(A parallel effect can be seen when taking acid suppressant medicines such as Proton Pump Inhibitors like Omeprazole. Also, after other stomach issues such as bariatric surgery.)
My CBC with differential showed normal sized RBCs. I understand they’d be abnormally large in the presence of B-12 deficiency.
I requested a reticulocyte study a few years ago, since anemia has been chronic. The cell populations were normal. I’ll request another one next week when I meet my GP on Zoom (or something more secure).
This is the most severe the anemia has been. I was in the mountains (2km above sea level) last weekend and I really noticed the effects.
Apparently normal sized RBCs can, and often do, occur in B12 deficiency.
The reason often being that the macrocytic effect is counter-balanced by a microcytic effect of iron deficiency. At least, sufficiently to keep RBC sizes towards the middle.
Have you got a Red cell Distribution Width result there? A high RDW can occur in this situation.
However, you are obviously aware as a reticulocyte study should be the next step.
It strikes me that concern and misunderstanding about TSH led this endo to overlook what is really important here
FT3 followed by FT4 are the important numbers
The latest FT3 and FT4 were midway into the second quartile. Previously they were below clinical range.
We aim to have results sitting roughly 75% through their respective ref ranges
This fabulously brilliant endocrinologist missed the important red flag...low Frees with possibly very low FT3.
Low T3 has possibly resulted in low GH and so impaired T4 to T3 conversion. She also missed the textbook symptoms of hypothyroidism.
Can you please post the actual FT3 and FT4 lab results, including reference ranges to verify this?
Cranking up your NDT would have raised the levels of the Frees .....which your labs showed was needed in the first place.
By accident you worked it out yourself..... more replacement hormone
You have been sent running round in circles looking for a clue that was available to you/ your endo at the start!
For good health every cell in the body must be flooded with T3 by way of a constant and regular supply.....this wasn't happening for you and the symptoms you experienced underlined that
After appeasing an endocrinologist worried about my suppressed TSH by a cunning lab trick - it doesn't say much for an endo who has to be appeased like this!
Until medics are taught correctly in med schools, and continue to focus on, and monitor treatment, based on TSH that lack of understanding will continue to leave patients struggling.
“Until medics are taught correctly in med schools, and continue to focus on, and monitor treatment, based on TSH that lack of understanding will continue to leave patients struggling.’
This new endocrinologist is “middle aged” and didn’t blink at my description of titrating the NDT. She pointed out that, when taking NDT, the high proportion of T3 suppresses FT4. This is perhaps another reason they prefer levothyroxine + Cytomel, as it can be administered in a “physiological ratio.” But, she allowed that many patients just don’t feel well taking levothyroxine.
The younger endocrinologists barely know how to palpate a thyroid and they’ve come to rely on TSH completely. They don’t care a whit about FT4, probably because they’re all consumed with treating diabetes, because of the high incidence of ultra-processed foods consumed here, and the stunning incidence of type two diabetes.
Thyroid patients, for the most part, don’t collapse into comas and die prematurely like diabetics. They don’t go blind or have toes and feet drop off. Thyroid patients wither slowly at home, out of sight.
Thyroid patients, for the most part, don’t collapse into comas and die prematurely like diabetics. They don’t go blind or have toes and feet drop off. Thyroid patients wither slowly at home, out of sight.
This is why we have so many people here.
No! The bottom line remains....
Until medics are taught correctly in med schools, and continue to focus on, and monitor treatment, based on TSH, that lack of understanding will continue to leave patients struggling.’
If med students were taught correctly then they would be able to diagnose the thyroid conditions causing ill health and treat them appropriately. For example, this endo failed to see the significance of....
The latest FT3 and FT4 were midway into the second quartile. Previously they were below clinical range.
Your argument details the effect....not the cause. But I think you are suggesting that they don't consider thyroid disease a serious problem so it's not a priority. How wrong they are.....again that is lack of education in med schools
I doubt that death certificates ever state " lack of T3" as a cause of death, but instead state conditions which are the result of lack of T3.
If the cause were to be timeously and correctly identified and treated then....
Thyroid patients would not be left to wither slowly at home, out of sight ......and this forum would become redundant.
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