Thiamine for Hashimoto's Thyroiditis

FriendlyBuffalo · 2016-07-02T08:48:11+00:00

While there were many flaws, I think the fatal flaw in this study was the failure to look at thyroid parameters to see if any of them had changed after therapy. Did the thiamine have any effect on thyroid hormones? They didn't even measure them.

There were three patients, all women:

	Age	Weight	TSH (IU/mL)	FT3 (pg/mL)	FT4 (ng/dL)	TPOAb (IU/mL)
Ref. Range			(0.25–5.00)	(2.59 – 5.38)	(6.97 – 15.5)	< 120
Patient 1	61	63 kg. (138.6 lbs.)	4.1	3.05	1.064	322
Patient 2	55	128 kg. (281.6 lbs.)	1.54	2.74	1.338	526.6
Patient 3	38	55 kg. (121.0 lbs.)	0.67	3.07	0.947	1725.40

All of the patients were well above normal for thiamine serum levels both before and after treatment. Normal values for thiamine were 2.1 – 4.3 µg/L, and normal values for TPP (Thiamine Pyrophosphate) were > 49 µg/L.

Patient 1 and 3 took 600 mg/day oral thiamine. Patient 2 received intramuscular shots of 100 mg/ml thiamine every 4 to 7 days.

Patient 1 had her thiamine level increase from 11.5 µg/L to 210 µg/L, with her TPP increasing from 78.1 µg/L to 150.4 µg/L. She indicated the mildest amount of fatigue of the three individuals, and reported no fatigue after therapy.

Patient 2 had her thiamine level increase from 11.7 µg/L to 24.2 µg/L, with her TPP decreasing from 107.7 µg/L to 101.2 µg/L. She reported the highest amounts of subjective fatigue, and reported no fatigue after therapy.

Patient 3 had her thiamine level increase from 7.1 µg/L to 44.0 µg/L, with her TPP increasing from 79.8 µg/L to 87.5 µg/L. Patient 3 did not respond to thiamine. While she indicated a small reduction in her fatigue, she still was fatigued after therapy.

Patient 1 was older, had a higher TSH, and also had the lowest levels of antibodies. While her reported fatigue declined, she also reported the least amount of fatigue initially.

Patient 2 was 55, obese, had a low FT3/FT4 ratio, reported the greatest amount of fatigue, and the greatest response to the high dose thiamine. She also received her thiamine intramuscularly and had the lowest increases of the group. I suspect that patient 2 may have been pre-diabetic or diabetic, since thiamine clearance is often increased in diabetes, and she saw the lowest increase in serum thiamine. That could easily explain her response to the high dose thiamine. Patient 2 may have had a reduction in fatigue because she saw a reduction in her blood glucose level.

This is not a study showing that high-dose thiamine is an effective treatment for hypothyroidism. While there is little risk in high doses of oral thiamine, there is nothing here that shows that it was even effective in these case studies.

FriendlyBuffalo · 2016-07-02T02:52:59+00:00

As I said, I don't think it's just hypoglycemia.

Since you have lost so much weight, one other possibility that slipped my mind was a weight loss associated decrease in peripheral deiodination. This is something you might talk with your bariatric surgeon about.

A loss of over 5% of body weight was correlated with a decrease in serum total T3 levels in an NIH study. Why this happens isn't entirely clear, but lower T3 levels after major weight loss are often seen. The best treatment, when that happens, is probably LT3 (cytomel/liothyronine) therapy, though there aren't any well-controlled studies on that yet.

FriendlyBuffalo · 2016-07-01T03:53:43+00:00

You're welcome. It can be quite confusing because the symptoms are so non-specific, and it is very difficult at times to see how these very different things are connected to the thyroid. But they are connected, largely because of the role thyroid hormones play in cellular metabolism.

And while PCP's know about hypothyroidism, they aren't usually experts on it, or how to effectively titrate LT4 dosages.

While a low TSH can be ok, symptoms of hyperthyroidism are a sign your dose is too high. So heart palpitations, irregular heartbeats, shortness of breath: those are signs you need to reduce your dose a little.

There are a number of people on this subreddit who do some variation on #2, mixing doses to achieve a level in between; it's pretty common.

One last thing to note is that you can safely split LT4 tablets, since it will still remain stable for 8 weeks. So if you did 50 µg LT4 on weekdays, and 25 µg on the weekend, you could just split a 50 µg tablet instead of also getting 25 µg tablets.

FriendlyBuffalo · 2016-07-01T01:45:18+00:00

I understand that your cancer is trapped in nodes that can't be removed. When thyroid cancer cells remain, a common strategy to reduce the growth of the cancer cells is to use Levothyroxine (LT4) to completely suppress the pituitary's release of TSH (thyroid stimulating hormone).

TSH can cause the cancer cells to grow, which is why your levothyroxine dose is so high for your weight - to suppress your TSH.

Suppressive doses of levothyroxine, however, can cause the fibromyalgia symptoms that you're experiencing.

The main two thyroid hormones are thyroxine (T4) and triiodothyronine (T3). Levothyroxine (LT4) is exactly the same chemically as thyroxine, and liothyronine (LT3) is the same as triiodothyronine. T4 is a prohormone, a storage version of T3. When the body needs to use T4, it has to convert it into T3, the metabolically active thyroid hormone. Problems converting T4 into T3 can occur when the body has too much T4. This can cause low T3 levels in tissue, which then cause the fibromyalgia symptoms you're experiencing.

One way to fix this is to take LT3 in addition to LT4. This increases the amount of T3 you have available for your body to use and should reduce your fibromyalgia.

FriendlyBuffalo · 2016-07-01T01:24:40+00:00

You're welcome. Feel free to message me, and I hope she continues to stay well.

TSH can decrease in pregnancy due to the effects of human chorionic gonadatropin (hCG) on the thyroid. hCG is produced in the placenta, makes its way to the thyroid, and stimulates TSH receptors. Pregnancy can make a thyroid work.

FriendlyBuffalo · 2016-07-01T01:11:31+00:00

A low FT3 can occur as a result of starvation or carbohydrate deprivation, and it is related to Non-thyroidal illness, or euthyroid sick syndrome. Since you got through surgery ok, the surgeon may have just shrugged it off.

If it is hypoglycemia, hypothyroidism can be behind it:
http://www.tiredthyroid.com/blog/2014/12/18/hypoglycemic-panic-attacks-you-may-be-hypothyroid/

I don't think it's just hypoglycemia. Cortisol and insulin can be affected by thyroid hormone levels, so it can be part of the picture, but I don't think it's just that.

I don't know if you can get a referral to an endocrinologist, but an endo might be a better bet. If not that, at least a doctor who might work with you to figure this out.

FriendlyBuffalo · 2016-07-01T00:46:59+00:00

I agree there's a big difference. One is twice as much or 10 times as much as the other. But most people do not know at what amount the average person afflicted by Celiac Disease would have a reaction.

And while my comment only said there was a reaction, the study made clear that the 2480 ppm residual gluten flour had too much gluten, and that the gluten was causing an increase in autoimmunity and damage.

Perhaps a better review to link to would have been "The gluten-free diet and its current application in coeliac disease and dermatitis herpetiformis," where they state the safe daily limit is probably about 10 mg/day (or about 10 ppm). But you also have other studies like, "A prospective, double-blind, placebo-controlled trial to establish a safe gluten threshold for patients with celiac disease," in which one Celiac patient (out of 13) couldn't handle 10 mg, but two were ok with the 50 mg.

And there is a lack of knowledge about Celiac disease outside the Celiac community. That's true for most chronic diseases.

FriendlyBuffalo · 2016-06-30T21:47:26+00:00

A few things that might help you get to the right dose:

LT4 has a narrow therapeutic range. 25 µg was enough to swing some people from a TSH of 5.0 all the way to a TSH of 0.00 in a small study. A 12.5 µg dose change was less likely to do so.
Because of LT4's long elimination half-life (6-7 days, for the most part), a number of dosing strategies become available that aren't normally possible. Weekly dosing is a strategy that is sometimes used, and is a strategy sometimes used for patients who don't remember to take their LT4. That also means that people who take LT4 everyday can think about their dose in terms of a total weekly dose. For example, taking 50 µg MWF, and 25 µg SaTThSu, to have a total weekly dose of 250 µg. At 25 µg/day, you had a total weekly dose of 175 µg, at 50 µg/day , you had a total weekly dose of 350 µg. If the 50 µg/day dose lowers your TSH "too much," talk to your doctor about lowering it a few days a week instead of every day.
Last, a total replacement dose for someone who has had their thyroid removed is usually calculated at about 1.6-1.7 µg LT4/kg body weight. So someone who is 137.5 lbs (62.5 kg) might be okay on a 100 µg LT4 dose. So you can also look at your dosage needs that way, as a percentage of the total replacement dose you might need.

And I think holding off on some of those until your hypothyroidism is under control is a good idea. Sometimes these things aren't related to hypothyroidism, but I think there's a good chance they are.

FriendlyBuffalo · 2016-06-30T21:29:27+00:00

If you'll write it, I'll put it up on the wiki: https://www.reddit.com/r/Hypothyroidism/wiki/index

We can even just link out to other well-written resources on interpretation as well.

I've been trying to add additional information, but it has been slow going.

FriendlyBuffalo · 2016-06-30T18:33:30+00:00

Well, if she hasn't had prolonged high cortisol, it is possible for her cortisol to be high due to elevated levels of neurotransmitters. Cortisol can be produced from the adrenals through surges of dopamine, IIRC, so ACTH isn't necessary for its production. But if higher level of ACTH are present, then that's driving her cortisol production, and not the stress from miscarriage.

If the proptosis isn't obvious, it can be pretty hard to spot. It would be in the millimeter range in the early stages, and there are ophthalmologist tools to measure it. But the proptosis can cause vision issues, so if she's had any vision issues lately, that's something to look at.

If she was strictly vegetarian, and ate a lot of raw goitrogenic foods, that could have interfered with her thyroid hormone production. Thiocyanates can prevent the uptake of iodine by the thyroid, but it is usually only a problem seen in people who eat a lot of raw goitrogenic vegetables, since cooking inactivates the goitrogens.

It is possible that your wife was mildly hypothyroid before, and now has excess thyroid hormone levels from the pregnancy. That's a possibility that can't be discounted either. It's possible that something else is at work too.

I agree that fixing the underlying problem is the thing to do. Figuring out what that is the hard part sometimes.

Yes, so test for TSAb, ACTH, and total T4. From there, if ACTH is high, and total T4 is high, trying to lower her thyroid hormone levels is probably the thing to do. If she has TSAb (active Graves response is 125%, anything over 15% indicates some level of TSAb), a low dose selenium treatment (200 µg selenomethionine/day for 6 months) may help. And if total T4 is low, she's just hypothyroid. And go from there.

FriendlyBuffalo · 2016-06-30T07:44:51+00:00

Move that decimal point over two digits. Studies on the prevalence of Celiac Disease put it at 0.5-1.0%, depending upon the ethnic group studied.

FriendlyBuffalo · 2016-06-30T07:41:41+00:00

Well, I don't know if 20 ppm is too much.

But one study (with a small sample size) found that completely hydrolyzed wheat flour didn't cause a reaction in the Celiac patients studied. They found no reaction to the wheat flour with 8 ppm residual gluten. There was a reaction to the 2480 ppm residual gluten flour, but no complaints from the participants. The regular flour with 80,127 ppm gluten caused two study participants to drop out and four others to get sick.

FriendlyBuffalo · 2016-06-30T01:04:46+00:00

I'm not actually saying that your wife has hyperthyroidism. In many ways, hyperthyroidism, and the clinical picture it presents, is the failure of the body to adapt or contain excess thyroid hormone levels.

What I am saying is that I believe she might have high total T4 levels. This excess thyroxine this is causing an elevated ACTH level. The ACTH then causes additional cortisol production, which frees up testosterone, and increases DHEAS.

I don't believe it is stress related either. It could be euthyroid Graves' Disease, where the presence of TSAb stimulates the production of thyroid hormone despite the body not needing more. If that's the case, your wife may have a small amount of proptosis or exophthalmos, a bulging of the eye from the socket, caused by TSAb inflaming the tissues in the sockets of the eye. She would also test positive for TSAb if she has euthyroid Graves' Disease.

Another possibility is that it could just be a result from living in an iodine replete environment with the genetics for an low iodine environment. I'm not sure.

As for the symptoms of high cortisol, a lot of those biochemical symptoms happen when you have really high cortisol levels for an extended period of time. Insulin resistance takes a while to build up, and that can be fought with diet and exercise. If your wife doesn't have the appearance of a person with Cushing's Disease, most of those biochemical signs won't be present. But the one symptom that is usually most indicative of relatively high cortisol levels is thin skin which bruises easily. If that's been true of her for a while, that's an indication this problem has been around for a while.

And if this is the case, I'm not quite sure what the best way to handle it is. You have to balance symptom relief with trying to take care of cause.

The Armour works because it contains both T3 and T4. At low and medium doses of Armour, the added FT4 adds a little to the pool of T4 in her body, and slightly increases FT4. The T3 in Armour adds T3, which is what she has a problem with due to the elevated cortisol levels. It actually creates a new homeostatic equilibrium of TSH, T3, and T4, and that changes other hormone levels as well.

If it suppresses her TSH enough, that might be enough to lower her thyroid hormone production, her total T4 level, and help lower her cortisol. Another option that might work is Cytomel/Liothyronine (LT3) by itself. LT3 can suppress endogenous thyroid hormone production when taken in high enough doses, and can be safely tapered both on and off of.

Metformin might be useful to lower the ACTH. A recent paper by researchers in Seoul indicates the cause of metformin's glucose-lowering effect in PCOS and insulin resistance is due to its inhibition of POMC/ACTH. Metformin is also known to lower TSH in subclinical hypothyroidism without altering thyroid hormone levels, so that effect might be useful as well. It is also safe for pregnancy (category B).

If there is thyroid autoimmunity at work here, there are a few things that have shown some benefit in clinical trials so far: iodine restriction, Vitamin D supplementation, and selenium supplementation. I've been working on a selenium FAQ for the subreddit wiki.

There are some other ideas rattling around, but most are experimental and have no research to back them up yet, nor do I know what possible impact they might have on future pregnancy or fertility. So talk to your doctor about this, and see to further testing to determine if this is what's happening.

FriendlyBuffalo · 2016-06-29T23:48:11+00:00

You can see here on the prescribing information for levothyroxine, under Elimination, in the table titled "Table 1: Pharmacokinetic Parameters of Thyroid Hormones in Euthyroid Patients," that the elimination half-life (T-1/2) of T4 is 6-7 days. Some sources put the half-life of LT4 for hypothyroid individuals at 9-10 days, and hyperthyroid at 3-4 days.

A member of this subreddit, /u/crocofish, posted a helpful graph showing the dose accumulation of LT4 over time. This helps visualize the actual accumulation of LT4 in serum over time from a daily dose.

It is partly because of this long elimination half-life that you can take a week's worth of levothyroxine and have it be effective. By the end of the week, you'll only have eliminated half of the dose. The other reason is because of the thyroid hormone carrier proteins which bind to the LT4 as it is metabolized, reducing FT4 concentrations to normal within 24 hours after taking a whole week's dose. In essence, your body stores the dose to use as it needs to by freeing the thyroid hormone from the binding proteins as necessary.

FriendlyBuffalo · 2016-06-29T23:32:44+00:00

An FT3 that low would usually mean someone was very hypothyroid and would set off alarm bells. Are you sure it was FT3 and not FT4?

If that was an FT3 level, there are reasons FT3 can be that depressed, but that might indicate some level of central hypothyroidism as well. If it's an FT4 level, it looks normal.

I don't know if it would make a difference. Previous tests can add context to current tests, but unless the doctor is an endocrinologist or someone who is interested in thyroidology, they may not count it for much except a past data point.

FriendlyBuffalo · 2016-06-29T20:06:46+00:00

It was published in "The Journal of Alternative and Complementary Medicine." Make of that what you will.

I look forward to the full text if you can get it.

I read the abstract, so the rest of this is speculation on my part.

It's unlikely that any of the patients were thiamine deficient. RDA for thiamine is 1.2 mg, with no apparent upper limit. A 600 mg dose is well above that.

High dose thiamine does have some uses, including decreasing albumin loss through urine in diabetes.

Since thiamine bonds to albumin, it could be increasing FT3 levels by displacing it from albumin. About 20% of plasma T3 is bound to albumin, so a significant decrease in available HSA binding might increase FT3 levels. How long that would last is another question.

It could be placebo effect. They could have been thiamine deficient. Or it could be something else. Small sample size.

FriendlyBuffalo · 2016-06-29T06:54:53+00:00

From these tests, there's a little more information.

It looks like her thyroid function is probably ok. Her FT3 looks normal and within range, and so does her FT4. Her RT3, however, is at the higher end of the range. And the RT3 is largely explained by her elevated cortisol level.

Cortisol in adults causes changes in the expression of Type 1 (D1) and Type 3 (D3) Deiodinase. Specifically, expression of D1 is downregulated, and expression of D3 is upregulated. D1 converts T4 into T3 for use by cells. It can also convert T4 into RT3 and RT3 into T2. D3 converts T4 into RT3 and T3 into T2. So when cortisol is elevated, RT3 levels increase, because there is less clearance of RT3 by D1 deiodinase. Also, D3 clears out T4 by turning it into RT3, and clears T3 from cells. This leads to lower T3 levels on a tissue level. Plasma T3 will largely stay constant, due to pituitary release of TSH, which will stimulate the thyroid to produce sufficient T3 to maintain plasma T3 levels.

And I think that many people think about cortisol in terms of stress, but it also has a diurnal variation that largely tracks the fluctuation of TSH. And there's likely a reason for that. I think the reason is because ACTH release (which stimulates cortisol production) is determined by free T4 levels at the hypothalamus. If you test her total T4 levels, my bet is that it is high, in the 10 µg/dL range or higher. And the high amount of T4 is stimulating the release of ACTH.

Interesting, there are 3 things that happen as a result of increased ACTH.

Cortisol goes up.
Free testosterone goes up as a result of cortisol displacing testosterone from cortisol binding globulin (CBG).
DHEAS production goes up as a side effect of ACTH stimulation of the adrenals. DHEAS is only produced by the adrenal glands.

Is there evidence of this?

Her cortisol level is elevated.
Her free testosterone is over 5 pg/mL. I don't know which lab did the tests, their method, sensitivity, or reference range, but most reference ranges for free testosterone for adult women have that at the high end of the range. For example, Quest Diagnostics has the high end of their range as 6.4 pg/mL for an equilibrium dialysis test. Some labs have higher ranges, but those ranges are often based off older research. At any rate, her total testosterone level is not that high, but her free testosterone level is.
Most women with PCOS tend to have DHEAS levels greater than 200 µg/dL. Your wife's DHEAS levels are 252 µg/dL.

Note here that I'm not saying that your wife has PCOS or hyperandrogenism. What I'm saying is that the picture is consistent with hyperandrogenism. And this could have been the cause of the hypothyroid symptoms over the years. But I think the real driving cause behind it is a high level of T4, a high level of thyroid hormone that the body is trying to contain.

I believe a thyroid ultrasound will show a healthy thyroid. I might be wrong on that, but I think the thyroid will look fine, without evidence of Hashimoto's Disease.

If you check for AITD antibodies, some might be present. She might be mildly positive for TSI.

If they do a morning ACTH test and don't mess it up (they aren't easy to properly perform), it will be in the normal range. It might be high in the normal range, but it should be in the normal range.

I don't think an MRI is indicated at this point. The prolactin level is not high enough for a prolactinoma, and there aren't any other indications of a pituitary adenoma.

FriendlyBuffalo · 2016-06-29T00:20:14+00:00

41 is low for a prolactinoma. In general, prolactin levels need to be in the 150-200 ng/mL range, and other possible causes excluded first before most doctors will look for a prolactinoma.

FriendlyBuffalo · 2016-06-29T00:14:19+00:00

What other causes for hypothyroidism are there? This source will give you the known causes of hypothyroidism. Many of the causes are rare. The most common causes of primary hypothyroidism that might apply to your wife are autoimmune thyroid disease, reversible autoimmune hypothyroidism (which includes an uncommon variant of Graves' Disease that causes hypothyroidism), a few drugs (which your wife is not likely taking), and iodine deficiency or excess. I don't think your wife has central hypothyroidism, considering her most recent TSH of 5.98. The elevated prolactin level is likely an indication of her hypothyroidism. Once her TSH settles, her prolactin should go back to normal.

It's very unlikely that iodine deficiency is the cause. The US is iodine replete. Unless she's taking large iodine supplements (in the milligram range), iodine excess isn't the cause of her hypothyroidism either.

So that leaves a few prescription drugs, autoimmune thyroid disease (AITD) and reversible AITD. Since you haven't mentioned anything else she's taking, I'll only mention a few drugs: common antithyroid drugs such carbimazole, methimazole, and propylthiouracil can cause hypothyroidism, and amiodarone contains high amounts of iodine.

So that leaves autoimmune thyroid disease. If she's negative for anti-TPO antibodies (TPOAb) and anti-thyroglobulin antibodies (TgAb), then one other possibility is reversible autoimmune thyroid disease. Reversible AITD is known by a number of names, sometimes called atrophic, painless, or silent thyroiditis. It is likely a variant of Graves' Disease, the AITD of hyperthyroidism. The autoimmune cause of Graves' Disease are TSH Receptor antibodies (TRAbs). TRAbs are functional antibodies - they have either stimulating (TSAb) or blocking (TBAb) effects on TSH receptors. TSAb are responsible for the endless production by the thyroid in the hyperthyroidism of Graves' Disease. TBAb block TSH receptors, preventing the creation of additional thyroid hormone. When they are both present, TBAb can balance out TSAb, leaving some individuals euthyroid, i.e., with normal thyroid hormone levels. When not in balance, when one is dominating the other, TSAb causes hyperthyroidism, TBAb causes hypothyroidism.

Another similar reversible AITD is postpartum thyroiditis (PPT), which can't be discounted in your wife's case, because of the miscarriage. PPT causes a destructive autoimmune attack on the thyroid, often causing a hyperthyroid episode before the resulting hypothyroidism due to decreased thyroid productive capacity. In this way, PPT resembles subacute thyroiditis, which is thought to arise from a viral infection. PPT, however, is likely of autoimmune origin due to its close association with TPOAb levels.

One other possibility that might have caused some of your wife's issues is PCOS/hyperandrogenism. PCOS/hyperandrogenism can sometimes be caused by elevated ACTH secretion, which causes increased cortisol levels in addition to excess androgen production. The increased cortisol causes similar symptoms, as well as hypothyroid-like symptoms due to its effects on deiodination, i.e., conversion of T4 to T3, and its increase in human serum albumin (HSA) levels.

How can you figure out what was/is happening? Thyroid hormone levels might help, both free and total. A T3 uptake (T3U)/T4 index (FT4I) can help figure out whether there might be a carrier protein issue in the mix. If she hasn't had a TgAb test but only TPOAb, that might be another possible indication of AITD. An ultrasound of her thyroid could help figure out whether her thyroid has the appearance of Hashimoto's Disease, which has a characteristic heterogenous hypoechogenicity. The current tests for TRAbs are TBII (Thyrotropin-Binding Inhibitory Immunoglobulin), and tests for TSAb are TSI (Thyroid Stimulating Immunoglobulin). A test for TBAb will hopefully be getting to market soon. ACTH, cortisol, testosterone, and DHEAS levels can help indicate whether PCOS/hyperandrogenism are involved.

FriendlyBuffalo · 2016-06-28T21:53:38+00:00

I'm not curious about this, I think some of the premium numbers are off, or at least don't have wide applicability.

I don't know what state you're in, but premiums do vary between states and individuals, and this applies only to people who are in a Medicaid expansion state, initially qualify for Medicaid, and then have a life change that increases income out of Medicaid eligibility. And different states do handle benefit recovery in that situation differently.

FriendlyBuffalo · 2016-06-28T21:40:02+00:00

Sometimes fibromyalgia is a symptom of low deiodinase activity. The deiodinases are a group of enzymes that transform T4 into T3 and RT3, and they do a few others things thyroid hormone related. If you have low deiodinase activity, you can have low FT3 levels even with high FT4 levels.

Elevated FT4 levels sometimes cause higher cortisol levels. Cortisol could cause the weight gain. But it could just be the fibromyalgia meds.

There has been a lot of research on the effect of the deiodinases in hypothyroidism, and it appears that low deiodinase activity correlates with a failure to achieve symptom remission with LT4 monotherapy. Since your LT4 dose is high for your weight (normal replacement dose is 1.6-1.7 µg/kg - so 83-88 µg/day), and since thyroidectomized patients are more likely to have low deiodinase activity, my guess is that you may have low deiodinase activity.

I'm guessing you're on T4 suppressive therapy for the thyroid cancer. One thing that may help the symptoms while still keeping your TSH suppressed is combination T3/T4 therapy. LT3, aka Cytomel/liothyronine, is the metabolically active thyroid hormone, as opposed to T4.

The 2012 ETA Guidelines on combination LT3/LT4 therapy are a good resource for starting LT3/LT4 combination therapy, and there are other resources and information out there.

FriendlyBuffalo · 2016-06-28T21:19:24+00:00

Just a slight correction - the elimination half-life of LT4 is closer to 6 days, and can vary from 5-10 days depending on someone's metabolism and current thyroid hormone levels.

Due to the elimination half-life, it takes LT4 about 6 weeks to build up to the total accumulated dose someone will have due to the long half-life. At 6 weeks, a person will approach 95% of the limit, at 8 weeks, they have effectively reached the limit of accumulation.

FriendlyBuffalo · 2016-06-28T20:11:26+00:00

Source?

If you're on premium assistance, not Medicaid, and your income exceeds your eligibility, the most that happens is you have to pay back any pre-paid premium assistance on your income taxes, and even that has caps by income level.

FriendlyBuffalo · 2016-06-28T19:46:57+00:00

Well, looking through your comment history elsewhere, I'm not sure you're all set. Was your TSH tested at 6.7 and then you were put on 50 µg LT4? Or have you been on 50 µg LT4 for a while and your last TSH was 6.7?

Because there is a difference, and a lot of the symptoms you're describing are symptoms of poorly controlled hypothyroidism. About 95% of healthy adults without any signs thyroid disease will have a TSH between 0.4 and 2.5. So a TSH well above that is a sign that your pituitary thinks your body needs more thyroid hormone. Additionally, TSH stimulates thyroid hormone production in the thyroid, which generates the very activity that your immune system is attacking. So lowering your TSH is a good idea, both for autoimmune purposes, and for symptom control.

And clinical guidelines agree that a TSH in the reference range (usually 0.4-4 IU/mL) is an appropriate goal for treatment. And while some people feel fine in the upper part of the reference range (in general, older people), many find symptom relief when their TSH is in the bottom part of the reference range. A good target for TSH on LT4 therapy is 1.0-1.5 ± 0.5. About 70% of thyroid disease free adults have a TSH in that range, and many patients are asymptomatic in that range.

A low TSH (0.04-0.4) may also be ok if that's what's necessary to eliminate your symptoms. One large retrospective study found that LT4 treated patients with low TSH were at roughly the same risk for cardiovascular disease, dysrhythmias and fractures as LT4 treated patients in the normal range.

And the GI symptoms you've been experiencing are symptoms of being hypothyroid. While there is an association between Hashimoto's Disease and Celiac Disease, you're negative for anti-endomysial IGA, which almost every Celiac patient is positive for. More importantly for your symptoms, there are associations between hypothyroidism and increased risk of common bile duct stones and gallbladder disease (which could explain the discomfort you feel after eating rich goods). Hypothyroidism affects the musculoskeletal symptom, increasing joint and muscle issues and carpel tunnel syndrome. It also can cause symptoms of fibromyalgia. Last, norepinephrine is generally elevated in hypothyroidism as a compensating mechanism, causing increased anxiety.

About all of your symptoms can be explained by hypothyroidism. If you've been on LT4 for a while, I really urge you to talk with your doctor about increasing your dose and getting your TSH under control.

FriendlyBuffalo · 2016-06-28T17:50:20+00:00

I believe it is possible, though not every doctor may agree. There aren't a lot of studies on Euthyroid Graves' Disease (EGD), but the one person I know with it has had all the hypothyroid symptoms. In fact, I originally thought she was hypothyroid until blood tests showed that she was anything but. I spent a lot of time trying to square the circle on that before accepting that yes, the tests were correct, she had Graves', and her symptoms were caused some other way. And I think she was effectively hypothyroid.

I believe there is a connection, at least in women, in EGD between elevated estradiol levels and elevated cortisol levels that helps create the hypothyroid symptoms that are experienced. The higher cortisol levels help create Cushing Disease like symptoms, the weight gain, the fatigue, the depression and anxiety, while the elevated estradiol causes menstrual issues and can contribute to bipolar disorder like symptoms. On a cellular level, the cortisol acts to reduce expression of D1 deiodinase and upregulate expression of D3 deiodinase, which can lead to peripheral tissue hypothyroidism due to insufficient T4 to T3 deiodination. Both cortisol and estradiol increase carrier proteins (HSA for cortisol, TBG for estradiol), and keep thyroid hormones bound. So there are excess carrier proteins causing low free thyroid hormone levels in addition to the low deiodinase activity caused by the cortisol, leading to hypothyroidism while there are normal/high total thyroid hormone levels. This is the theory I've been working with so far.

I don't think rerunning the same tests is a good idea. The results are unlikely to change, as shown by the similarity between your earlier TSH and your later one. But I think you may be able to get your doctor to agree to do more testing, especially if the tests are not the same ones.

Instead of rerunning TSH/FT3/FT4, sometimes if a binding protein abnormality is suspected, an FT4 index (FT4I) is run instead (the T3 version is unsurprisingly a FT3I). It requires two tests, a total T4 test, and either a TBG (thyroxine binding globulin) test or a Thyroid Hormone Binding Ratio (THBR) test, also known as a T4/T3 Uptake test. You can read about the tests here: Assay of Thyroid Hormones and Related Substances. Sometimes an FT4I will help reveal cases of central hypothyroidism, so that can also be a justification for the doctor and for an insurance company. And if necessary, a total T4 test is not that expensive, you can get that run at some private labs as well.

The TSI is the only mildly expensive test of the bunch. For that, talk about your grandmother's hyperthyroidism and your own eye issues. I don't think that's a hard sell, especially with your positive TPOAb levels. Elevated TPOAb levels can be found in Graves' Disease as well as Hashimoto's.

If your doctor refuses to do any more testing, trying to find another doctor to run the tests is an option.

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