SPINA THYR a research tool to evaluate thyroid function, deiodinases activity, TH resistance

[Gondwanaland]

Here is an analysis of kelp trace elements (I searched quite a bit... ). This is by dry weight (as you see from the moisture content).

Thanks for your hard work
However I think they should have provided the Bromine amount

 

[Iritu1021]

I can only refer to my personal experience:

Hair test back in 2013 showed Iodine very high and Lithium very low.

How on earth would I have very high iodine levels? I don't live at the coast and don't consume seafood often. The salt is iodized, that's it. And I have Hashimoto's.

If I drink lithium-containing water I immediately feel hypo symptoms (I get cold hands and feet), so I have no intention of supplementing with Li.

My husband doesn't have thyroid problems or CFS but he started supplementing with iodine out of curiousiy and felt a boost of energy on it. We did his hair test and just got the results today: his iodine levels came back toxic through the roof (also for selenium which he taking along with iodine). So once again, I only see a direct link to excess intake and no evidence for inverse correlation.

One can get quite a bit of iodine from iodized salt. Also, iodine deficiency actually appears to be more prevalent in coastal areas, which was counter-intuitive to me but it has something to do with coastal soil depletion. Iodine also comes from bread and dairy. My guess is that in Hashimoto's it would also be released into blood from thyroglobulin destruction or from the deiodination of supplemental thyroid hormones.

There are some clearly documented problems with increased iodine intake.

1. In 1996 iodized salt was introduced in China, which resulted in increased iodine consumption. In a 1999 a study reported an increase in the incidence of autoimmune thyroiditis, overt hypothyroidism, and subclinical hypothyroidism in three regions of China. As their iodine intake increased, the incidence of thyroid conditions increased proportionately.

2. A more recent study which examined the Chinese population also showed that the incidence of subclinical thyroid disorder was higher in areas of the country(Rongxing and Chengshan) in which iodine consumption was higher. (3) In Ronxing area, higher iodine intake was attributed to higher iodine concentration in drinking water there. In addition to an increase in the incidence of hypothyroidism in this area, the incidence of autoimmune thyroiditis was also higher.

Mercola writes on his blog about a study that showed even 400 mcg of supplemental iodine per day can lead to subclinical hypothyroidism.

Clearly, iodine is one of the most controversial and debated topics in thyroid community. We each have choose for ourselves what side we want to bet on.

 

[Lolinda]

There are some clearly documented problems with increased iodine intake.

1. In 1996 iodized salt was introduced in China, which resulted in increased iodine consumption. In a 1999 a study reported an increase in the incidence of autoimmune thyroiditis, overt hypothyroidism, and subclinical hypothyroidism in three regions of China. As their iodine intake increased, the incidence of thyroid conditions increased proportionately.

2. A more recent study which examined the Chinese population also showed that the incidence of subclinical thyroid disorder was higher in areas of the country(Rongxing and Chengshan) in which iodine consumption was higher. (3) In Ronxing area, higher iodine intake was attributed to higher iodine concentration in drinking water there. In addition to an increase in the incidence of hypothyroidism in this area, the incidence of autoimmune thyroiditis was also higher.

Mercola writes on his blog about a study that showed

The following website contains a list of several such studies in different countries:
https://thyroidnation.com/iodine-crucial-harmful-hypothyroidism/
(Some links dont work any more)
All studies have the same outcome: autoimmune thyroiditis went up from iodine fortification of salt. But I don't think this means that iodine is dangerous or such because the problem can be avoided using selenium. - so the argumentation goes, with reference to research.

 

[Iritu1021]

The following website contains a list of several such studies in different countries:
https://thyroidnation.com/iodine-crucial-harmful-hypothyroidism/
(Some links dont work any more)
All studies have the same outcome: autoimmune thyroiditis went up from iodine fortification of salt. But I don't think this means that iodine is dangerous or such because the problem can be avoided using selenium. - so the argumentation goes, with reference to research.

Please let us know how it goes with iodine!
My anti-TPO went up on it from 75 to 220 - and I was taking selenomethionine - but it could've been due to something else or maybe the increased antibody production is just a marker of increased thyroid enzyme activity. I still think low dose iodine is worth a try.

 

[Lolinda]

I come back with results on thyroid and orthostatic probs.

I'm so glad there is someone else out there who believes in POTS - thyroid connection!

So, what was this connection? The pathomechanism is: thyroid ➞ arterial stiffness ➞ decreased cardiac output ➞ some contribution to any type of orthostatic issues. Details:

To anyone with orthostatic issues, here a few lines why thyroid is so important:

• Decreased cardiac output is a major factor in orthostatic intolerance (Example: Table 2 on page 19 in this research shows the low values in POTS)
• Thyroid is a reason for low cardiac output (reference): "Thyroid hormones have a variety of effects on the cardiovascular system that can greatly impact cardiac function (Figure 1). Hypothyroidism is associated with decreased cardiac output due to impaired relaxation of vascular smooth muscle and decreased availability of endothelial nitric oxide. This produces a cascade effect of increased arterial stiffness that leads to increased systemic vascular resistance" ............ "Cardiac echocardiography has demonstrated impaired relaxation in patients with overt and subclinical hypothyroidism. .... diastolic dysfunction from impaired relaxation."

The above addresses me 100%: I have POTS, lowish cardiac output, decreased availability of nitric oxide, increased systemic vascular resistance and diastolic dysfunction

All the above in one simple sentence: in order to find out if thyroid probs could be contributing to whatever orthostatic probs, test for arterial stiffness. So, I did a hell of hunting for doctors until I found the one and only doc in a nearby city who had devices for arterial stiffness. He is a researcher who really understands his business. Measured my arteral stiffness using two different devices:

• sphygmocor - this is the gold standard
• Mobil-O-Graph NG - this is a simple, cheaper, new device, but ok

Result: I have no arterial stiffness at all. Now, if you have orthostatic issues or have low cardiac output, what can you take away from all this? The following was my learning: The problem is the lack of professional devices. Asking doctors is where I wasted time. The winning method was: pretend I am a doctor and call manufacturers. They tell me med device vendors. Show interest. Finally say: I would like to approach the purchase slowly. First send my patients to someone who has the device. Whom do you recommend? It was as simple as google a little and do 4 phone calls! Here is the list of devices: Devices are on the market that measure arterial stiffness parameters (augmentation index, pulse wave velocity). These include Complior, CVProfilor, PeriScope, Hanbyul Meditech, Mobil-O-Graph NG, BP Plus (Pulsecor), PulsePen, BPLab Vasotens, Arteriograph, Vascular Explorer, and SphygmoCor

@sb4 @Mary @Emootje @BadBadBear [USER=31864]@debored13[/USER]

 

[sb4]

@Lolinda Very interesting but also confusing. You still have POTS, yes? but no arterial stiffness?

 

[Iritu1021]

All right guys, I finally summed up the whole SPINA thing on my blog - in two parts!

http://www.chronicfatiguediagnosis.com/2018/05/29/spina-model-going-beyond-tsh/

 

[Iritu1021]

I come back with results on thyroid and orthostatic probs.


So, what was this connection? The pathomechanism is: thyroid ➞ arterial stiffness ➞ decreased cardiac output ➞ some contribution to any type of orthostatic issues. Details:



All the above in one simple sentence: in order to find out if thyroid probs could be contributing to whatever orthostatic probs, test for arterial stiffness. So, I did a hell of hunting for doctors until I found the one and only doc in a nearby city who had devices for arterial stiffness. He is a researcher who really understands his business. Measured my arteral stiffness using two different devices:

• sphygmocor - this is the gold standard
• Mobil-O-Graph NG - this is a simple, cheaper, new device, but ok

Result: I have no arterial stiffness at all. Now, if you have orthostatic issues or have low cardiac output, what can you take away from all this? The following was my learning: The problem is the lack of professional devices. Asking doctors is where I wasted time. The winning method was: pretend I am a doctor and call manufacturers. They tell me med device vendors. Show interest. Finally say: I would like to approach the purchase slowly. First send my patients to someone who has the device. Whom do you recommend? It was as simple as google a little and do 4 phone calls! Here is the list of devices: Devices are on the market that measure arterial stiffness parameters (augmentation index, pulse wave velocity). These include Complior, CVProfilor, PeriScope, Hanbyul Meditech, Mobil-O-Graph NG, BP Plus (Pulsecor), PulsePen, BPLab Vasotens, Arteriograph, Vascular Explorer, and SphygmoCor

@sb4 @Mary @Emootje @BadBadBear [USER=31864]@debored13[/USER]

I'm not sure if arterial stiffness is a good measure of POTS. My problem is vein hyper-elasticity due to EDS, and when it comes to T3/T4/T1AM is seems to primarily affect my microvacular organ beds, at the junction of arterioles-venules since there is mismatch in the pressure between the two. In other words, it appears to be the problem on the level of capillaries rather than large blood vessels that would be implicated in arterial stiffness. I've read that some rheumatology doctors in the old days used some device to judge capillary perfusion in the nail beds. I don't have such a device but just looking at my nail perfusion gives me a pretty good idea (do they look pink all the way, do they have a glossy shine to them or look dry, cracked and splinted, etc.)

That being said, I do admire you ingenuity with getting what you need @Lolinda !

 

[Lolinda]

I'm not sure if arterial stiffness is a good measure of POTS

Stop stop stop! Nobody ever claims arteriat stiffness to be any measure of POTS. The measure of POTS is supine-standing heart rate difference, I guess we all agree on that. What I wrote above means:

• arterial stiffness may be a contributing factor to orthostatic probs
• A connection from thyroid to orthostatic probs goes like this: thyroid probs can cause arterial stiffness, can cause low cardiac output, can contribute to orthostatic probs
• To test this connection (AND NOT TO MEASURE POTS!) test arterial stiffness

You still have POTS, yes? but no arterial stiffness?

Exactly.

some rheumatology doctors in the old days used some device to judge capillary perfusion in the nail beds

I highly appreciate all thoughts you posted above. I thought so many times there must be something in this direction. Whatever you find out about this device, please let me know. Do you have the original source you read? Quantifying things by a device can be so much more valuable than guessing "hm this looks to me well-perfused.... or, is it?"

My problem is vein hyper-elasticity due to EDS,

I am very curious, how was your vein elasticity diagnosed? (and how your EDS?)

 

[Mary]

The following was my learning: The problem is the lack of professional devices. Asking doctors is where I wasted time. The winning method was: pretend I am a doctor and call manufacturers. They tell me med device vendors. Show interest. Finally say: I would like to approach the purchase slowly. First send my patients to someone who has the device. Whom do you recommend? It was as simple as google a little and do 4 phone calls!

Great detective work!

Actually I did something similar several years ago when trying to find a doctor who had an impedance cardiography machine, but it was simpler - I just called the manufacturer (did not pretend I was a doctor) and asked for names of doctors who had purchased their machine, and they willingly gave me some names. But at times it might be useful to pretend one is a doctor, will keep this method in mind!

 

[Iritu1021]

Stop stop stop! Nobody ever claims arteriat stiffness to be any measure of POTS. The measure of POTS is supine-standing heart rate difference, I guess we all agree on that. What I wrote above means:

• arterial stiffness may be a contributing factor to orthostatic probs
• A connection from thyroid to orthostatic probs goes like this: thyroid probs can cause arterial stiffness, can cause low cardiac output, can contribute to orthostatic probs
• To test this connection (AND NOT TO MEASURE POTS!) test arterial stiffness

Exactly.

I highly appreciate all thoughts you posted above. I thought so many times there must be something in this direction. Whatever you find out about this device, please let me know. Do you have the original source you read? Quantifying things by a device can be so much more valuable than guessing "hm this looks to me well-perfused.... or, is it?"

I am very curious, how was your vein elasticity diagnosed? (and how your EDS?)

EDS is a clinical diagnosis and I had two geneticists who signed off on mine. Some people do have genetic mutations for it but I didn't test positive for any of the known ones but it's not required. The diagnosis is made on clinical history alone. I've always been highly flexible (a body made for yoga) and I can push my thumb down to reach my arm (forgot the name of what this test is called), I had severe pelvic vein distention after pregnancy, leg vein reflux... But what I do not believe that EDS caused my CFS and dysautonomia, it just accounted for my individual presentation of it. I still sometimes get orthostatic HR increase of 20-30 but now I hardly notice it. All the bad stuff (like sympathetic overdrive) that got blamed on POTS and EDS was actually thyroid related (both too low and too high) and now completely resolved.

 

[Iritu1021]

here's the link to assessing joint hypermobility. Now I remember it's called Brighton Score. Mine wasn't super high but enough to qualify.
https://www.ehlers-danlos.com/assessing-joint-hypermobility/
I'm posting this only for academic interest since as I said earlier EDS diagnosis did absolutely nothing good for me. Treatment with midodrine ended up a total disaster.

 

[Lolinda]

Actually I did something similar several years ago when trying to find a doctor who had an impedance cardiography machine, but it was simpler - I just called the manufacture

I would like to learn from you: could you tell me about names of such machines? And, which ones are good / are the gold standard?

did not pretend I was a doctor)

Nice to live in a culture where patients are accepted as a conversation partners... and you do not need tricks pretending this or that... Here people are conservative and the only worthy partner to talk with is a doctor... damn...

assessing joint hypermobility. Now I remember it's called Brighton Score. Mine wasn't super high but enough to qualify.

Thanks for all your detailed test descriptions! Good to know that you got the same as I did... I always appreciate it to learn how other people were tested to see if I got the right thing. Always watch if those doctors are doing right!!

I am very curious, how was your vein elasticity diagnosed?

Such a pitty that you didnt get any test for vein elasticity!!! this was my main question.... because I have never-ever seen a test nor any publication that EDS actually causes increased vein elasticity! Have you seen anything? It looks to me that this is a generally accepted and indeed plausible "internet-knowledge" which is devoid of any actual proof / test ever!!
(the thing measured and proven is that Marfan causes aortic distension in some, but that has not anyhow anything to do with POTS...)

 

[Iritu1021]

I would like to learn from you: could you tell me about names of such machines? And, which ones are good / are the gold standard?

Nice to live in a culture where patients are accepted as a conversation partners... and you do not need tricks pretending this or that... Here people are conservative and the only worthy partner to talk with is a doctor... damn...


Thanks for all your detailed test descriptions! Good to know that you got the same as I did... I always appreciate it to learn how other people were tested to see if I got the right thing. Always watch if those doctors are doing right!!

Such a pitty that you didnt get any test for vein elasticity!!! this was my main question.... because I have never-ever seen a test nor any publication that EDS actually causes increased vein elasticity! Have you seen anything? It looks to me that this is a generally accepted and indeed plausible "internet-knowledge" which is devoid of any actual proof / test ever!!
(the thing measured and proven is that Marfan causes aortic distension in some, but that has not anyhow anything to do with POTS...)

Yes, I think they've stretched out that theory quite a bit to imply that everyone who has flexible joints has abnormal veins. Most of people with EDS who are extremely hypermobile have no POTS, and most people with POTS do not have EDS.
I think it's more likely that in dysautonomia there is a genera defect in collagen production due to hormonal and nutritional deficiencies.
@Lolinda, how did your iodine experiment go?

 

[Mary]

I would like to learn from you: could you tell me about names of such machines? And, which ones are good / are the gold standard?

Hi @Lolinda - unfortunately, as far as I can tell, these machines are no longer made. They were called "Bio Z Machine" and the company which made them was bought by another company several years ago, and the new company decided not to make them (!) which is really too bad. I think you can find refurbished machines on-line though I don't know how good they are.

Here people are conservative and the only worthy partner to talk with is a doctor...

Well, a lot of people here believe that too! But I think things are changing as patients are becoming so much more educated about their health - or maybe it just seems that way to me since I see so many knowledgeable people on this board!

 

[Iritu1021]

I finally kept on my promise to deliver a list of drugs and supplements that affect peripheral deiodinastion. Phew - that was quite some work there!
If anyone has anything else to add there, please let me know.
http://www.chronicfatiguediagnosis.com/2018/06/04/peripheral-deiodination-table/
http://www.chronicfatiguediagnosis.com/2018/06/04/peripheral-deiodination-table/

 

[Gondwanaland]

@Iritu1021 Thank you so much, awesome!

The last item should be flavonoids?

Would lowered D1 explain my worsening and increased anti-Tg ab from taking vit D?

 

[Iritu1021]

@Gondwanaland It's hard to tell what the net effect of Vitamin D would be since it affects both deiodinases in different directions. If it decreased you liver metabolism than it could potentially have an indirect link on autoimmunity or circulating antibodies.

 

[Gondwanaland]

I read from unreferenced sources that PUFAs inhibit hormone release from the thyroid gland because they inhibit proteases.
Coconut oil is said to enhance T4 >>> T3 conversion.

Do you know anything about it?

 

[Iritu1021]

I read from unreferenced sources that PUFAs inhibit hormone release from the thyroid gland because they inhibit proteases.
Coconut oil is said to enhance T4 >>> T3 conversion.

Do you know anything about it?

@Gondwanaland I remember you and I talked about PUFAs in the past about PUFAs, and if I remember correctly I think I found a legit reference on that, at least for linoleic acid. I know that Peat says it's true for both omega-3 and omega-6. I felt more hypothyroid on high dose PUFAs and I know you did too.

As for coconut oil, it's very high in saturated fat so it falls under my "high fat diet" tab. When I was extremely sick after abruptly stopping high dose NDT, I nourished myself back to life by drinking young coconut smoothies. I had a really strong craving for it and it felt right for my body. I've always liked coconut and I never liked fish so I guess my body does have have a pretty good innate understanding of my metabolism!