Author: L S-L (Page 2 of 2)

FOR THE THYROID NEWBIE

Basic guide for you who are new to thyroid issues

I wanted to make the guide I wish I had had. Way back when, more than 20 years ago. Knowledge that could have saved me a lot of suffering. Maybe I would have been more healthy today.

So it is my hope, this info will help you. Of course, there is so much info today, compared to earlier. But maybe there is too much info for someone new to this. I hope I can make it,if not easy, then at least possible to understand.

I don’t know how you are feeling at present. If you have just been diagnosed with hypothyroid, with autoimmune thyreoditis, have had your thyroid removed or maybe you are struggling to get a diagnosis. Maybe your doctor is dismissing you, but you feel sick and know something is wrong.

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ESTROGENS IN MENOPAUSE, time to change the recommendations?

Translation from an article by E.F.Eriksen, M.H.Moen, O.L. Iversen,

This is a translation of an article published in the Norwegian Journal for Physicians, Tidsskriftet, https://tidsskriftet.no/2018/03/kronikk/ostrogener-i-menopausen-p%C3%A5-tide-endre-anbefalingene

New studies show, that  treatment with estrogen with start before age 60, are for the most part positive.  It’s time to change the recommendations.

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REVERSE T3

Abstract

Reverse T3 is not the big bad wolf in our thyroid system. It is a necessary brake where FT3 is the gas pedal. We can get too much RT3 when we take more T4 medicine than we are able to convert to T3. Could be just too high dose, or that we don’t convert well. Other conditions can increase RT3 too much as well. It’s a good idea to test RT3 from time to time. But it is not necessary to test all the time. 

I will look at myths and misunderstandings around RT3. for one thing, RT3 does not block T3 by occupying T3 receptors. Nor does it hinder T4 to T3 conversion. If there is a big bad wolf, it’s deiodinase 3, D3. It’s D3 who converts T4 to RT3, and who hinders T3 from attaching to the T3 receptors i the cell nucleus. 

But there are no “wolves” in our thyroid system. Only participants with their own roles to play. And the better we understand the play, the more can we hopefully optimize our thyroid levels and feel better. 

I will look at what causes too high RT3, and what one can do bring it down. 

There is so much talk of reverse T3 these days. A few years back, we didn’t even know what RT3 was. And our knowledge of it is still very sketchy. There are many misunderstandings out there. I find the attitude towards it is more balanced in Norway compared to the US. They do test for it in Norway. But not in Sweden. And in Denmark, I don’t think neither patients or doctors know what it is for the most part.

I find, that in many of the US Fb groups, they regard RT3 as something one should have as little of as possible. One adheres to some values that one claims is absolute.  Like STTM, Stop The thyroid Madness, who claims, one should not have more than 2 digits from the bottom range. That is, if range starts on 10, one should not have over 11, maybe 12. This is BS. RT3 must be seen in conjunction with the FT3. Quite apart from the great variations one sees in ranges across the world. As you will see below, the Norwegian range is much more narrow and starts on 4 ng/dl!

We need Reverse T3

Reverse is not something one rather should not have. It’s the brake in the car. Without the brake, things would go very wrong. FT3 is the gas pedal, and the two must work together. I usually have confidence in DR. Westin Childs. But when he explains RT3′ role as the body’s brake in times of extreme stress, then I begin to wonder, link to Dr Childs article on . RT3. RT3 is made all the time, every day.  We have RT3 at all times. When we are under extreme stress, serious illness and so on, much more T4 is being converted to RT3. RT3’s function is to balance our thyroid system. In times of acute illness, it’s function is to reduce our metabolism to conserve energy.

STTM refers to Kent Holtorf’s site and what he writes about RT3. They write about the equation Dr. Childs also give as a good indicator of what is a normal level of reverse. I believe that equation is quite sensible. It’s very simple. You take FT3 and divides with RT3. The number needs to be over 0,20.

2 digits above lower range is BS

Where it goes wrong, is when STTM writes, we don’t need that equation anymore, we need only think about not being over 2 digits from bottom of range. This is totally mistaken, and very exaggerated. It all depends on your FT3. If you have low FT3 and high reverse, then you are in trouble. But if you have a high FT3 and a reverse T3 midrange, then you might have no issues.    

I see many people in the US consider this to be a rule. They don’t understand, RT3 and FT3 must be seen together. I have had angry pm’s from admins in thyroid groups for saying, this with 2 digits over bottom range is not correct. It has become one of the dogmas. The focus is not on learning and figuring out this thyroid thing together, but on being right. Some of these admins have anger issues.  One wonders, if their FT3 might be too high. I have even gotten flak for writing to a person who had just started on thyroid meds, on NDT, that she did not have a big reverse problem like the admins claimed. Her RT3/FT3 ratio was 0,19. They said, she must not take the NDT, but start on T3 only. I wrote, the T3 in the NDT will most likely clear up that reverse in time. I got some long pms from the admins, they would have none of it. It would be laughable if it weren’t for the fact, they make people scared and worried. I can’t be bothered with groups like that. You don’t have a big reverse issue with a ratio of 0,19. You have an issue, and you need to follow up on it. but it is not a BIG problem. And how many who have just started on thyroid meds are confident to take only T3 meds? Not many.

 My Norwegian tests are in pmol/L for the FT3 and in nmol/L for the RT3. 5,9 pmol/L FT3 and 0,28nmol/L RT3 (0,14-0,54). The reference range in other countries is often ng/dl. My 0,28 nmol/L equals 8 ng/dl. I would say that is a quite low RT3. Still, my ratio is only 0,21. I don’t know how well that equation works. The Norwegian range is 4-15.5 ng/dl. A common range elsewhere is 8-25 ng/dl. So the Norwegian range is much more narrow. 

Kent Holtorfs claims about Reverse T3

I have gotten most of the info in this section from Thyroid Patients Canadas’ article “RT3 inhibits T4-T3 conversion. How worried should we be?”, link to article . Tania Sona Smith sees through Holtorps claims on the very negative impact of RT3 in this article. I believe it is his claims that is the basis for the somewhat hysterical attitude towards RT3 in the US. 

Holtorf says on his post on RT3, that RT3 is a very powerful inhibitor of the T4 to T3 conversion. He refers to a study by Chopra from 1977, link to Chopra’s  study. Chopra experimented with rat’s livers and kidney tissue, which he soaked in T4 hormone. Holtorp describes Chopra’s study like this:Most endocrinologists believe that reverse T3 (rT3) is just and inactive metabolite with no physiologic effect, which is not the case, however. This study and subsequent others demonstrate that rT3 is a more potent inhibitor of T4 to T3 conversion than PTU (propylthio­uracil), which is a medication used to decrease thyroid function in hyperthyroidism. In fact, rT3 is 100 times more potent than PTU at reducing T4 to T3 conversion. Clearly, rT3 not just an inactive metabolite. The authors conclude, “Reverse t3 appeared to inhibit the conversion of t4 to T3 with a potency which is about 100 times more than PTU…

Holtorf’s big mistake

Notice the dots at the end of his last quote “100 times more than PTU…” Sonia spotted that, and read Chopra’s study herself. and what did it say? The ending of that sentence, is “on a molar basis”. What does that mean? It means that 1 mg of RT3 inhibits 100 times more than 1 mg of PTU. But do we have RT3 in similar doses as PTU in our bodies? We do not. In fact we have very, very little. Tania quotes a study by Wiersinga’s where he estimates a daily RT3 production between 23-100 nanomoles/L. 100 nanaomoles/L is 65 mcg. And that is actually twice as much as a normal daily amount of RT3. In this article, they estimate we produce app 28 mcg a day, https://www.frontiersin.org/articles/10.3389/fendo.2019.00856/full . That is not the point here. I just didn’t want you to think we make that much RT3 a day. That must be in cases of acute illness. 

65 mcg or 28 mcg, it’s very, very little. Keep in mind, 1 mg is 1000 mcg. Now we want to compare this to the PTU. What is a common daily dose of PTU? It’s between 50 and 1200 MG. So between 50 000 and 120 000 mcg! And you claim, RT3 is a stronger inhibitor?

RT3 inhibitory effect on the T4 to T3 conversion is very very small.  

We must hope Holtorf has just overlooked this, not realized it. Though you would think, a doctor would know the difference between milligrams and micrograms. Anyway, his conclusions are not correct. They have unfortunately had a great, negative impact on the thyroid community. I see a T4 fear in many thyroid groups on Fb, especially in the US. People are being told, they must not have a higher than midrange FT4 when on T4 mono therapy. Otherwise you will get high reverse. You can, but not everybody gets a high reverse. Not at all. And with a midrange FT4, you don’t have enough T4 to convert to T3. You cannot get the around midrange FT3 you need. 

I never see that at least. I have seen it a few times. It’s usually someone in the beginning phase of their disease. We thyroid patients seldom have a convertion ratio over 30. Whereas healthy people almost always have a convertion ratio well over 30.

Then people are being told, you need T3 medicine. Because they even claim, on T4 meds, you need to have FT3 in upper range. Which you don’t. Please read my post on optimal levels and convertion ratio here

I don’t have anything against T3 medicine, or NDT. Not at all.  I use only NDT myself. But if you don’t really need it, and could do well on the T4, then I don’t see any reason for it. In many places in the world, it is hard to get, and  expensive.  So if it is not really necessary, then you might create a lot of stress and worry for no reason. And that is one thing that is not good for our health. Not everybody do well on T3 either. Many get issues with palpitations and maybe feeling nervous. I do myself on synthetic T3. Our own T3 will always feel more comfortable than any T3 we take.

Does Reverse T3 block T3?

No, it does not. Everybody writes it and says it. I have written it many times. But we have all been mistaken. Tania Sona Smith at Thyroid Patients Canada clarifies this issue, https://thyroidpatients.ca/2019/11/14/deiodinase-type-3-plays-a-t3-blocking-function/

Reverse T3 does not hinder T3 from entering the cells, it does not occupy T3 receptors and does not hindre T3 from attaching to them. 

Studies show, it is deiodinase D3 that do the blocking of T3. If you want to read up on the deiodinases and what they do, you can do so here. D3 is the deiodinase that converts T4 to RT3 and T3 to T2. It isn’t really that we have too much RT3, we have too high D3 activity.

Does it make a difference?

Yes, it does make a difference. We need to know if and when D3 dominates. 

D3 can still dominate even when RT3 is low. In those instances where our T4 is too low for there to be converted a lot of RT3, D3 can still inactivate T3 to T2.

D3 is like a soldier patrolling the outer boundaries of the cell, inactivating hormones as they enter. but when the body wants to lower the T3 level, then it moves towards the cell nucleus and stops T3 from  entering the nucleus.

RT2? Yes, it is a thing, 3,3’T2, Reverse T2. There are many thyroid hormone metabolites. Triac, several T2’s, T1. Lots we don’t know about yet, things that need to be studied. So there are many things that can potentially affect our thyroid levels. so we should not get too hung up on the Reverse T3.

D3 does not block T3 receptors via RT3. What it does, is move towards the nucleus in cells that express D3, and quite simply hinders it from entering the nucleus by converting it to RT2. 

Can RT3 bind to T3 receptors?

No, it can’t. Neither RT3 nor RT2 can bind to hormone receptors in the cell’s nucleus. RT3 lacks an Iodineatom in a key position, and can’t bind to a T3 receptor. RT3 has less than 1 % affinity to bind to a T3 receptor,  Bolger, M. B., & Jorgensen, E. C. (1980). Molecular interactions between thyroid hormone analogs and the rat liver nuclear receptor. I cannot link to the study, as it is in a journal. But you can see a table from the study here:

Table 1

As you can see, where T3 has 100% affinity for binding to T3 receptors, RT3 has 0,189 % affinity. So it has no blocking function, like som many claim. Including Holtorf and Westin Childs. 

When a thyroid hormone lacks an Iodine atom in this placement, in the inner ring, then it is inactive. It is called “inner ring deiodineation”. You can see where the Iodine atom is “missing” on the figure below. 

Figure 1

What causes D3 dominance?

Deiodinase 3 will dominate and RT3 will increase when your thyroid levels are too high in any given tissue.

The body decides what is too much. 

  • What is the righrt level changes suddenly in case of acute disease. The body then wants to lower hormone levels to conserve energy.

You can have too much T4, T3 or both.

Pooling

When one is dosing with T3, high D3 activity can become hidden.

  • Even if one has too low T3 levels inside cells and tissues, it might not result in lower FT3 levels in serum blood. As long as one fills up on T3 every day. This is what we patients call pooling.

What causes high RT3?

Too much T4 medicine

For us hypothyroid, the most common cause of high RT3 is too much T4 medicine compared to one’s conversion. One can have high FT4levels without issues if one converts well. But if one doesn’t convert well and take too much T4 medicine, then RT3 can become too high.  And when one in many countries not even can have Free T3 measured, so that one not even know one does not convert, then one can get to feel real bad, maybe for years. If you can’t have Free T3 taken where you live, do yourself  favor and buy an online test. Thank God, we have many on line labs nowadays. You can read more about T4 medicine and things to keep an eye on here

If you have FT4 in upper third of range, and still do not have FT3 around midrange, then you convert poorly. You can also divide FT3 with FT4. The number you get should lie over 0,24. Under, and your conversion is not good enough.  For instance, FT3 5 pmol/L divided with FT4 10 pmol/L = 0,26. Good conversion. Way too low FT4 though.

Under 0,24, and you will in most cases need some T3 containing medicine. Unless  raising the T4 dose will suffice. 

Figur 2, Burman et al.

You can seeit  in figur 2. In the two columns to the right, you see RT3 leveles on a low and a high dose T4 medicine 50 and 400 mcg. You can see, RT3 is much higher on the high dose.  And on a low dose, a hypothyroid person does not have enough T4 to make RT3 from. It’s the same for the unmedicated hypothyroid. BUT 400 mcg is a mega dose. Not many take that much T4 medicine. But it does tell us something about the tendency, at least. FT3 should have been included as well.

Non thyrodeal illness (NTIS)

Like I have mentioned above, in case of acute illness, the body loweres it’s metabolisme in order to save energy. FT3 can get low, RT3 increases while FT4 can stay normal. FT4 can also decrease. TSH can stay the same, become a little elevated or go down. 

I have gotten the info in this section for the most part from this article “Abnormalities of Thyroid Hormone Metabolism during Systemic Illness”, link to the article

 

How the TSH level can be very misleading 

Why does not TSH always become elevated as FT3 decreases? 

It’s because the pituary and the hypothalamus protects themselves by having a very high D2 activity. That is, these organs supply themselves with sufficient T3. That is one reason why diagnosing and dosing solely on the TSH level is very wrong. TSH does not always tell us how hormone levels in body tissue are. It’s quite common that it does not.

Deiodinase activity during NTIS

In studies on people with acute, life threatening diseases like cardiac ischemia and septic shock, one finds that there is lowered D1 activity in liver and body muscluature, increased D2 activity in body muscluature and incresed D3 activity. The combined effect of less T4 to T3 conversion and the increased T4 to RT3 conversion leads to low T3 and high RT3. On top of that, we get lowered thyroglobulin levels. Which leads to decreases in the totale T4 and T3.  

One often sees increased levels of cytosines in these conditions. And increased cytosines are correlated with lower thyroid hormone levels.

But acute illness is not the only instance where one sees NIT. One sees it in varying degrees in chronic disease as well. Which means that many conditions can contribute to an increase in reverse T3.

Non thyrodeal illness in different clinical settings

NTI can manifest in many, less critical conditions. Here is a table with various conditions and how they affect thyroid levels:


Total T3 Free T3 Reverse T3 Total T4 Free T4 TSH

Caloric deprivation  or ↓
Heart failure  or ↑  or ↓  or ↓
HIV infection  or ↓  or ↓  or ↓
Renal diseases  or ↓  or ↑
Liver diseases  or ↑  or ↑  or ↓
Pulmonary diseases  or ↑
Diabetes mellitus  or ↑  or ↑
Psychiatric illnesses  or ↑  or ↑

: normal.
↑: increased.
↓: decreased.

Figure 3

Calorie restricted diet

The decrease in thyroid hormones that one sees with fasting and dieting, is connected to the fact that the body goes in saving modus plus less Leptin. One sees FT3 decreasing, while FT4 goes up temporarily. During the first 2 weeks, RT3 increases. But normalizes again after that time. The normalization of RT3 is because FT3 is now lowered. The increase in RT3 is caused by less deiodinase, not increased conversion of T4 to RT3. This statement is a mystery to me. How is RT3 made except from conversion of T4 to RT3? The fall in T3 is caused by less conversion of T4 to T3. Less ATP (small monecules transporting energy to the parts of the cells that need it) can give less uptake of T4 in the liver, plus less deiodinase in tissues.

Leptin plays a crucial role. Leptin levels fall in concordance with the weight loss. If one takes Leptin one does not see the low thyroid hormone levels.

I don’t know that much about Leptin, but will be studying it. And write about it. But what is important, is that RT3 increases only the first 2 weeks. After that it is low FT3 that is the problem. I think we can conclude, low calorie diets are not the best for us hypothyroid.

HIV infection

When having HIV, one also gets a form of NIT. FT3 becomes low. But there is no increase in RT3. Thyroglobulin increases as well as the disease progresses. They can also acquire an actual hypo thyroidisme as pathogens infiltrate the thyroid. Much like Hashimotos thyroiditis. 

Heart disease

Our thyroid levels are of utmost importance for our heart’s functioning. They govern the heart’s rhythm, minute volume, systemic vascular resistance and how much the heart contracts (inotropism). When having a heart attack, T4, T3 and TSH falls, and RT3 increases.     

Renal disease 

The kidneys play a crucial role in our thyroid hormone conversion and excretion. App 20% of our thyroid hormone conversion takes  place here. With individual variations. So no wonderm that people with renal disease get low thyroid hormone levels. One does not see increased RT3 levles, but lower FT3 and thyroglobulin can also become lower.

Liver disease

The liver is the main organ when it comes to conversion T4 to T3, synthesizing of thyroglobulin, uptake of T4 and second most important when it comes to excretion of T4 and T3 into the blood stream. I would think it was the organ releasing the most  T3, but this is what it says.  One often sees thyroid levels affected with cirrhosis of the liver, Hepatitis and chronic liver disease.

Seeing as the liver is so important for our thyroid levels, it’s a good idea to take good care of it. The most beneficial for the liver, is giving it a rest. If you don’t eat any fat for 2, 3, 4 weeks, eating only greens and fruits, it starting cleansing itself.  

Many herbs are also helpful. I have taken heaps of Milk thistle and Artichoke. And many recommend them for us thyroid sick.But, turns out, they are not so good for us. I fell over this study, link to study on Milk thistle. We have 3 main thyroid hormone transporters. Our thyroid hormones cannot get into our cells except through those. MCT8 is one of those transporters. Silymarin (active ingredient in those herbs )inhibits T3 uptake by this transporter. Other studies show that Silymarin is good for other aspects of thyroid function. But all in all, probably better to use some other herbs. 

Bitter compounds are very important for our liver and gall function. In China and India they are well aware of this, and include something bitter in all meals. It’s only here in the West we don’t understand this. Maybe except France. But we knew it in earlier times. Bitters were much used to aid digestion. 

What can we use instead of Silymarin containing herbs? Dandelion is good, as well as Turmeric. Coffee enemas can also be helpful. Dr Hulda Clarks gall bladder flush is very harsh. I have done it 4 times. Never again. 

Diabetics

Diabetics often have abnormalities in their thyroid levels. Some studies have shown decreased TT3, Total T3, levels, and in some cases also decreased TT4. One sees also increased Reverse T3. I see some thyroid sites claim that this is because of badly regulated glucose levels. One has also found that it can have to do with inflammation, something called proinflammatory markers, like IL-6. This is beyond the scope of this article, but it is interesting. 

Ferritin and Reverse T3

There are several studies showing a correlation between hypo thyroid  and low iron levels. This study, study ironlevels and the thyroid in young Iranian girls also shows a connction between low ferritin and reverse T3. You will find a graph in the study. It\s not like you get very high RT3 from low ferritin, but there is a connection.  

Cortisol

I see they write on all thyroid sites, that stress and high cortisol will give you high RT3.  They write, high cortisol lowers T4 to T3 conversion, and increases T4 to RT3 conversion.  But no one refer to any studies on the subject. I can\t find a lot of studies on it either. I did find a study on people who are seriously injured. It\s really on seeing the effect of Selenium supplementation in the days after injury, if that would help with the NIT. They have this graph, and it looks like higher cortisol makes for less RT3:  

Figure 4, Mette M.Berger

 

I don’t know what is correct. I find it strange that there is so few studies on it, one would think it would be important. If you have some, please send me an email. 

Here ia another study showing HIGHER thyroid levels as cortisol level increase. It’s a study on sheep fetuses.Yes, I know. It’s weird. But that is the way it is in the world of science. There are lots of studies on hormones done on fish, for instance.  Here is a link to the study, https://pubmed.ncbi.nlm.nih.gov/2607090/. Then again, a study showing a connection between high cortisol and high Reverse T3, link to the study. It’s a study on people who have suffered a myocardial Infarction. It shows a greater increase in RT3 and decrease in T3 in the patients with higher cortisol. I cannot get access to the study though, I have just read the abstract. These people have just had a heart attack. I don’t know if the results can be generalized. 

Anyway, we need to know more about the connection between high cortisol and increased RT3. If there is any.  

How can we bring too high Reverse T3 down?

When one has too high RT3, one has too much T4 in relation to T3. They way to bring it down, is increasing intake of T3 compared to T4. If one is on T4 mono therapy, adding some T3 would be a good idea. If one has a high RT3, then taking only T3 for a period is a good idea. But if you have had no experience with T3 medicine, this will probably be too scary for you. Or maybe difficult in relation to your doctor. Few doctors would go along with this. You might have to settle for T4/T3 combo. Hopefully, the added T3 will bring RT3 down over time. If you are already taking T3 with T4, then maybe you would feel up to taking T3 only for a few days. I would join one of the T3 groups on Facebook and ask advice there. One would need at least 40 mcg  T3, divided over 4 to 5 doses.  Otherwise, just decrease the T4 dose and or increase T3, depending on how your thyroid levels are.  I am no expert on this, having never done it myself.  

If you are on NDT,  then adding some synthetic T3 would be the normal solution. 

Dr. Childs is concerned with doing something with the underlying condition. The high RT3 could be caused by inflammation. I am sure he is right.

But I don’t know how much of the RT3 is caused by simply overdosing with T4 or overdosing compared to not converting, or things like inflammation. So one needs to look at one self and one’s blood tests to determine this. If you have success with bringing RT3 down with T3 medicine, and make sure to not take more T4 medicine than you can convert, that is, rather add some t3 medicine if FT3 is too low. And you still get high Reverse T3 again later. Then I would think you can assume there are some other, underlying causes.  

It’s important to make sure to have good levels of the nutrients necessary for conversion. Selenium and Zinc are the two most important. All the three deiodinases are seleno enzymes. So without Selenium, they don’t work. You can read Dr. Childs post for more info, see link above. 

Conclusion

I hope this has cleared up some misconceptions around RT3. I find that Tania Sona Smith of Thyroid Patients Canada has done an important work on this. There have become many myths on this subject, people just repeat something without really investigating it themselves. I have had admins in groups telling me, science is not to be believed. These must be people who are not able to judge a study, to see if it is valid or not. And in stead of investigating each study, just dismissing science as a whole. It’s a bad strategy, just simply dismissing studies as irrelevant. Adhering to some fixed, inflexible ideas. We must always try to be open minded, ready to admit, we were wrong or mistaken about something. We just need to learn more and more.

 So thanks to Tania for doing that job. Many don’t think to see what science has to say. I don’t have a religious relationship to science, like some people seem to have. There is lots of bad science on the thyroid. for one thing, the participants are more often than not, under dosed. But when it comes to the physiology of our thyroid, and how it functions, then I believe we can trust the science.  Must trust it.

THE IODINE PROTOCOL

As with LDN, I am no expert on Iodine. I am on it myself, have been for about 6 months here in may 2020. I will be updating the post as I go along. I will be absolutely honest about what is happening. I won’t be writing too much about the complicated aspects of Iodine. But I want to present some of it. So if you are mostly interested in the more practical aspects and concrete tips, scroll down to “The Protocol”.

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HAS NDT GONE BAD?

NO, NDT hasn’t gone bad. That is the short answer. I take NDT myself, and it works just fine.

I see people claiming, NDT is no good anymore. That it is better to take synthetic T4/T3 now. I think this is very serious, that this incorrect, untrue info is being spread in the Facebook groups. It stems from STTM, Stop the Thyroid Madness, and its Facebook group, Adrenal Fatigue and Thyroid Care. STTM is a site that has contributed so much, and I am sad to see, there is such black and white thinking going on. This issue isn’t black and white.

I wrote to the woman behind STTM about this, Janie A. Bowthrope. I told her, we are lots of people who do great on NDT here in Scandinavia. She said, most of those who still “believe”  they are ok on NDT, only experiences adrenalin! I find that to be a strange claim. What does it mean? Adrenalin? We don’t have good thyroidlevels? We just think we do? A female admin in the Facebook group, told me in a comment, we here in Scandinavia probably took our meds right before labs! None of us know how to do our labs (?) I am a member in thyroidgroups  in many countries. The members in the Norwegian groups are among the better informed in the world, as far as I am concerned. I am aware that many thyroid patients don’t know how to do labs correctly. Norwegians on NDT are not among those.

It’s a little difficult to take this seriously. Yes, absolutly, there were some bad batches of Nature Troid in 18. It didn’t take long before there were good batches again. STTM claims, that NP Acella is bad now. We don’t have NP here in Scandinavia, I don’t know if they have it in other European countries. But i see lots of people saying it is fine for them, in the US groups. Just now, May 2020, I see people here in Scandinavia saying, there is something wrong with Erfa. With the smelly product Erfa themselves have made a statement about it. Erfa says, they contain the proper amount of hormone. But some experience it differently.  

So I am not saying, there are no issues. But to say, all NDT has gone bad, and to accuse the producers of being callous and indifferent to us patients and only out to make money, as Janie Bowthrope does here, https://stopthethyroidmadness.com/2019/09/23/the-sad-saga-of-where-we-are-today-as-hypothyroid-patients/  That is a sad saga.

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SYNTHETIC T4 TO NDT CONVERSION

How do I convert my T4 dose to NDT?

This is a question one sees often in the thyroid Facebook groups. There is a lot of confusion and insecurity around this. Which is not so strange, as there is very little good info on the topic. Here are my recommendations

The conversion tables the NDT (thyroid) producers themselves provide are ridiculously low. They are wrong, wrong, wrong. I don’t understand how they think at all. If they do. Think. One would be seriously under dosed if adhering to those guidelines. And if one’s doctor reads them, one could get serious problems. I don’t know how many doctors read these instructions. I hope they don’t. Here is a table from Nature Troid as a (bad) example.  

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CONVERSION, DEODINASE

I have translated some of Thyroid Patients Canada’ articles on conversion into Norwegian. These articles are very interesting, esp this one, https://thyroidpatients.ca/2019/11/12/the-basics-of-thyroid-hormone-action-transport-and-conversion/      

Most of the hormone conversion, T4 to T3 happens outside the thyroid. though there are big individual differences how much.  There are 3 enzymes responsible for this conversion, D1, D2 and D3. They do a lot more than convert T4 to T3 though.

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FT3 UPS AND DOWNS IN T3 THERAPY

This is not really a post. I have translated Tania Sona Smith’s article, https://thyroidpatients.ca/2019/11/25/free-t3-peaks-and-valleys-in-t3-and-ndt-therapy/ , into Norwegian.  For every Norwegian page, I want there to be a corresponding English, and vice versa.

This is just a presentation of Tania’s piece. She is looking into the reseach on how Ft3 behaves after dosing with T3 containing medicine.  Actually, there is not really any good studies on the subject . There is a study on FT3 after a single dose of T3. But that is not what most people take when dosing with T3. We do multidoses. There is no study on FT3 when multidosing, but there is one on T3, that is total T3. Where I live in Denmark, we cannot have FT3 tested. The endoes have forbidden it, they claim, FT3 fluctuates too much, it cannot be trusted. How do they know? With no studies? Anyway, FT3 and T3 follow each other in most instances . With a very important exception, when we take estrogen orally. Then both T4 and T3 becomes higher and FT4 and FT3 lower. So  VERY important to have the frees tested.

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TRIAC

This is just a short abstract of Thyroid Patients Canada’s article on Triac, https://thyroidpatients.ca/2020/01/02/when-dosing-t3-you-get-higher-levels-of-triac/ . I just want to draw your attention to this metabolite. The quistionmark on the image, is meant to signify my surprice when learning of Triac. I had never heard of this thyroidhormone metabolite until I read Tania’s post. It is quite strange, as it has been studied since the 1950ies. I don’t think many of our doctors have ever heard of it.

So what is it? It is a thyroidhormone metabolite like FT4 and FT3 are. It acts much as FT3, it’s abbreveration is TA3. It has a much shorter halflife than FT3, about 6 times faster.

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