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

[Gondwanaland]

Your dizziness might have been from POTS, did you check if you had an orthostatic change in blood pressure or pulse upon change from laying to standing?

It seemed to be just excess serotonin.

I am considering amitriptylin due to insomnia. Not sure if my liver can handle it though.

 

[Learner1]

Try citrulline or ornithine - they finally got me to sleep through the night.

 

[Gondwanaland]

Try citrulline or ornithine - they finally got me to sleep through the night.

I just read a review warning against Ornithine due to shingles reactivation

 

[Learner1]

Arginine can encourage herpes reactivation, so I stay away from it, and take lysine, which discourages it. My labs show I'm deficient in citrulline and ornithine, so I think I need them.

I take blanket internet advice with a grain of salt.

 

[Iritu1021]

https://www.ncbi.nlm.nih.gov/pubmed/27156111
@pattismith speaking of deoiodinase regulation by ubiquitination - this article may explain what happened to @Gondwanaland and many others on high dose iodine...

 

[Iritu1021]

https://www.ncbi.nlm.nih.gov/pubmed/27156111
Do low carb or gluten-free diets work through the change in deiodinase expression?

 

[Iritu1021]

here's the link to Vitamin A
https://www.ncbi.nlm.nih.gov/pubmed/19233213

 

[pattismith]

https://www.ncbi.nlm.nih.gov/pubmed/27156111
@pattismith speaking of deoiodinase regulation by ubiquitination - this article may explain what happened to @Gondwanaland and many others on high dose iodine...

this is an amazing paper, thank you for sharing!

"Increased D2 ubiquitination suppresses the activity of D2, causing a decrease in negative feedback of the hypothalamic-pituitary-thyroid axis."

excess iodine increases D2 clearance in the pituitary, so there is less T3 in the pituitary and then TSH increases, leading to hyperthyroidism!

https://www.ncbi.nlm.nih.gov/pubmed/27156111
Do low carb or gluten-free diets work through the change in deiodinase expression?

iritu, it isn't the right link

 

[Iritu1021]

And here's probably why omega supplements made two of us here worse, and why Ray Peat intuitively recognized them as bad for himself (I trust his observations more than his explanations).

Eur J Endocrinol. 1994 Apr;130(4):417-21.
Drug competition for intracellular triiodothyronine-binding sites.
Barlow JW1, Curtis AJ, Raggatt LE, Loidl NM, Topliss DJ, Stockigt JR.
Author information

Abstract
A variety of substances, including frusemide, non-esterified fatty acids (NEFAs) and non-steroidal anti-inflammatory drugs (NSAIDs), can compete for triiodothyronine (T3)-binding sites in serum and at the cell surface. We examined the competitive potency of these agents at intracellular T3-binding sites in order to assess their potential to act as T3 antagonists. Competition for [125I]T3 binding was determined using hydroxyapatite separation in cytosols and nuclear extracts prepared from livers of Macaca fascicularis. The T3 affinities were 15.8 +/- 1.2 nmol/l in cytosol and 0.23 +/- 0.02 nmol/l in nuclear extract. Dose-response curves were analysed by a four-parameter sigmoid curve-fitting program to determine competitor potency. The nineteen agents tested included various NSAIDs, NEFAs, non-bile acid cholephils (NBACs), frusemide, amiodarone and the flavonoid EMD 21388. In nuclear extract the most active competitors were linoleic acid (8.5 mumol/l) and linolenic acid (7.8 mumol/l). Potencies of NSAIDs varied between 66 mumol/l (meclofenamic acid) and 525 mumol/l (diclofenac). In cytosol, NEFAs were less potent but NSAIDs were stronger competitors than in nuclear extract. Half-inhibitory potencies in cytosol were between 13.2 mumol/l (meclofenamic acid) and 63.1 mumol/l (flufenamic acid). The NBAC bromosulphthalein was one of the most potent inhibitors in both cytosol and nuclear extract. When expressed relative to T3, diclofenac was a more effective competitor in cytosol than it was in nuclear extract. Amiodarone and EMD 21388 were without effect both in cytosol and nuclear extract. Frusemide (759 mumol/l) was weakly active in cytosol only.(ABSTRACT TRUNCATED AT 250 WORDS).

PMID:

8162174
[Indexed for MEDLINE]

 

[Lolinda]

Hey guys... this thread is running so incredibly fast.... guess what I am sick .... I am happy to see you all have so much energy.... so here I will reply to a few old comments:

I need some other people with POTS to help me figure out if I'm close or not. Maybe you can let me know if you fit into one of my descriptions and what your SPINA shows to help me sort it out better.
http://www.chronicfatiguediagnosis.com/2018/03/20/thyroid-inferno-the-eight-circles-of-hell/

I am back from a journey and now I will install this software these days and then you will hear from me. I am very interested in finding out if there is a connection of thyroid and POTS. In fact it is my priority 1 "path of attack" right now. And I think we have a much better chance to succeed if we collect a bunch of people with POTS and thyroid issues and compare.

@Lolinda
I have the same issues as you and my POTs is very extreme; after standing for 5 mins my HR increases by 30 pts and my BP drops. The slightest activity leaves me feeling like I've run a marathon including sitting with feet on floor and talking.
Have you found a treatment that helps your POTs.

If your BP drops upon standing, then you have orthostatic hypotension and no POTS. 100% sure. This shouldnt sound like some academic nuance, but it is a really important distinction to make. It is the very definition of POTS to have a >30BPM increase in HR without a drop in BP. I send you this because you will have better chances of finding similar people using the right term...
Having said that, here some detailed descriptions of what helped me with POTS:

• choline
• daily 1h of exercise (if needed seated or even laying. I started doing a few minutes per day! increasing by minutes! See this research for details on this POTS training method.) + vitamin D resolved my highly pathologic A1 adrenergic antibodies. Addition: I do not know which of these two measures was effective... or both together. I felt better.

 

[Iritu1021]

Hey guys... this thread is running so incredibly fast.... guess what I am sick .... I am happy to see you all have so much energy.... so here I will reply to a few old comments:



I am back from a journey and now I will install this software these days and then you will hear from me. I am very interested in finding out if there is a connection of thyroid and POTS. In fact it is my priority 1 "path of attack" right now. And I think we have a much better chance to succeed if we collect a bunch of people with POTS and thyroid issues and compare.


If your BP drops upon standing, then you have orthostatic hypotension and no POTS. 100% sure. This shouldnt sound like some academic nuance, but it is a really important distinction to make. It is the very definition of POTS to have a >30BPM increase in HR without a drop in BP. I send you this because you will have better chances of finding similar people using the right term...
Having said that, here some detailed descriptions of what helped me with POTS:

• choline
• daily 1h of exercise (if needed seated or even laying. I started doing a few minutes per day! increasing by minutes!) + vitamin D resolved my highly pathologic A1 adrenergic antibodies

I'm so glad there is someone else out there who believes in POTS - thyroid connection! I've tried to communicate about SPINA tool to some POTS community represntatives and have been completely shut down with "it has been proven that there is no connection between thyroid function and POTS". I don't know proven by whom or how - nor do I really care. It seems to me that specialists who know a lot about POTS do not know anything about thyroid complexity which means they are not the people in the right position to answer this question. We all definitely need to join our forces to over-ride the current level of bias and resistance on the issue.

I don't really have any meaningful drops in my blood pressure (except when Fluorinef gave me cerebral edema) but I use my overall blood pressure ranges to gage my thyroid levels (SBP 110 vs 120 is different states) and I pay attention to whether my DBP goes up with standing (also a sign of changed state). I also closely watch my tissue perfusion based on my hair, nails and visible blood vessels (such as under my eyes) and I noticed that based on thyroid levels (or T3/T4 ratio) I can be either underperfused or overperfused which goes against their grain that one is permanently fixed in either "low flow" or "high flow" POTS.

Look forward to hear what you find out with SPINA!

 

[sb4]

vitamin D resolved my highly pathologic A1 adrenergic antibodies

Very interesting. As far as I recall, on our last conversation you said you got your levels up to around 50ng(???) but didn't notice a difference. Did you end up going higher?

 

[Lolinda]

A request to all:
Would you help to improve PR?
When I checked back to this thread now, I simply lost track of which messages I wanted to reply. I went to the "Alerts" menu hoping to see who on this thyroid thread quoted me, replied to me, etc. But I did not find the old alerts because the Alerts menu contained only the last few days! This is really really stupid. This is inhibiting the very purpose of PR to create valuable discussions.
➞ I posted a request for improvement here:
http://forums.phoenixrising.me/inde...-and-i-cannot-react-fast-to-all-i-want.58416/

Please support my cause by posting there a message or two on how you perceive this problem or how you envision a better solution, etc, so they see that there is interest! Thanks.

Very interesting. As far as I recall, on our last conversation you said you got your levels up to around 50ng(???) but didn't notice a difference. Did you end up going higher?

Will answer privately. This is a loooong topic and I want to respect this thyroid thread by @pattismith by keeping off-topic messages short. (And eliminating my POTS-antibodies was done with a few drops of vitamin D. Maybe 1200 IU or so and was not related to my varied attempts to get my vit D levels up. That was much later!)

 

[Iritu1021]

Reading the SPINA article which pattismith informed me was just published this week.

https://www.frontiersin.org/files/A...00097-HTML-r1/image_m/fendo-09-00097-g002.jpg

"A recent study with chemically induced hypothyroidism in rats showed a more severely reduced tissue T3 than serum FT3, averaging 1–6% of the baseline versus 30%, respectively. In other words, the finding of slightly decreased circulating FT3 and perhaps also FT3 levels in the lower reference range may reflect the tip of the iceberg of the genuine T3 deficits in target tissues."

I'd be interested to see how well my T3 and fT3 levels correlate with each other. Maybe more thyroid dysfunction is being used in CFS after the switch to testing free hormone only.

I also started another thread yesterday about low hypothalamic T3 causing torpor state in animals. Sadly, I think I understand what "torpor" means. There was a time when I believe my hypothalamic (or general limbic area T3) dropped so low, it really felt like a state of near paralysis... That's what it looked like (according to what I read bears don't hibernate, they go into torpor...)

 

[Gondwanaland]

TSH increases, leading to hyperthyroidism!

I have had hyper symptoms with high TSH!

here's the link to Vitamin A
https://www.ncbi.nlm.nih.gov/pubmed/19233213

So the bottomline is vit A will up or lower thyroid function, depending on how long it is taken?

 

[Iritu1021]

I have had hyper symptoms with high TSH!

So the bottomline is vit A will up or lower thyroid function, depending on how long it is taken?

It is supposed to up-regulate deiodinase I activity in thyroid gland itself. Look at the table here.
I didn't read it the way you did. To me it reads like it just took longer for one form of Vitamin A to make a difference than another.

Looks like this might only be true for active form Vitamin A, beta-carotene probably won't work. I'm curious what was your experience on Retin-A?

I noticed I have a lot of night vision problems which could be consistent with Vitamin A deficiency.

 

[Gondwanaland]

I'm curious what was your experience on Retin-A

So far I have only tried one supplement which makes me feel awful (I suspect the soy oil in it). Otherwise I just eat liver 1x weekly. And CLO 1x which I forgot to take again.

 

[Iritu1021]

So far I have only tried one supplement which makes me feel awful (I suspect the soy oil in it). Otherwise I just eat liver 1x weekly. And CLO 1x which I forgot to take again.

My bad, I thought I remember reading that you tried prescription Vitamin A (isoretinoin). I guess it was someone else.

Yes, it's hard to tell if your problem were due to omega-6 or Vitamin A. Could it have been due to your thyroid getting activated and starting to secrete too much T4 and brain and/or other tissues not being able to convert it?

You also may not have D1 problem. Have you tried running your deiodinase SNPs? All of my D1 genes are abnormal, my D2 is not as bad though it has been in the past iatrogenically deactivated by high T3 doses (see the table in my previous post).

SNP rsID Minor Allele Genotype Phenotype
DIO1 rs11206244 T TT +/+
DIO1 rs2235544 A AA +/+
DIO1 rs4926616 T TT +/+
DIO2 rs12885300 T CC -/-
DIO2 rs225014 C CT +/-
DIO3 rs945006 G TT -/-
SNP? rs1190716 T CC -/-

 

[Iritu1021]

I just read a review warning against Ornithine due to shingles reactivation

Going back to T1AM - ornithine decarboxylase is thought to be the primary enzyme involved in T1AM synthesis. Ornithine might induce it.

 

[Gondwanaland]

My bad, I thought I remember reading that you tried prescription Vitamin A (isoretinoin). I guess it was someone else.

I did and Accutane as well, just didn't know the name Retin-A, sorry

es, it's hard to tell if your problem were due to omega-6 or Vitamin A. Could it have been due to your thyroid getting activated and starting to secrete too much T4 and brain and/or other tissues not being able to convert it?

I think excess vit E which antagonizes vit A
I didn't had excess T4, for the 1st time my TT4 levels were below range and FT4 very low in range.

Have you tried running your deiodinase SNPs?

I will check them out

Going back to T1AM - ornithine decarboxylase is thought to be the primary enzyme involved in T1AM synthesis. Ornithine might induce it.

I will have to look up what T1AM is.