How does low T4 affect B2 transport for those of us on T3 meds?

[BadBadBear]

The more I read about the importance of B2, and sufficient thyroxine to activate it, the more I wonder what happens for those of us who take exogenous T3 and have suppressed T4 levels?

My T4 levels are usually at a trace amount. I have tried switching to NDT, and even tried going mostly off of T3 meds to let my T4 levels come up. Even when I was on a minimal T3 dose (12 mcg per day) my T4 level stayed suppressed. When I took NDT, my body never seemed to take up the T4 and use it.

In both cases, I developed a very hypothyroid state and had to go back on straight T3. My NMH issues go crazy when I get low on thyroid hormones and my brain fog reaches dangerously ditzy levels. My NDT trial ended when I drove the wrong way down a street, thinking it was a 1 way street.

If I am taking one of the Source Naturals active B2 tablets, is this enough to compensate for the lack of thyroxine? Do the regular B2 supplements do anything useful if T4 is low? Is there anything else helpful that can be done?

Thanks!
Michelle

 

[Misfit Toy]

I have no thyroid and can't take T4, NDT or anything T4. I find it upsetting, but I am on T3 only. That's all my body can take. It stinks.

 

[BadBadBear]

I have no thyroid and can't take T4, NDT or anything T4. I find it upsetting, but I am on T3 only. That's all my body can take. It stinks.

@Misfit Toy - What are your issues when you try adding some T4?

I think T3 is the only thing that keeps me going, glad to have it available but I wish my body could use T4 appropriately.

 

[Misfit Toy]

What are your issues when you try adding some T4?

For me, I have MCAS. So, it totally fires that right up. I have hives from it and horrible itching. But also, I feel crazy on it. Absolutely nuts. Once I got up to 60 mcg, I couldn't sleep one wink. It was churning my heart, I was having a reaction to it. Every single NDT, compounded thyroxine, all if it. They told me you can be allergic to it. BS. I was dying on it.

Having said that, for me, T3 is not the answer. I am exhausted on it. I have no thyroid so therefore, no choice.

 

[Gondwanaland]

I am having trouble tolerating my thyroid replacement (T4+T3). I suspect copper deficiency (anemia is present, but plenty of iron).

After several months chelating copper from the joints (bursitis) with chondroitin + glucosamine + MSM, high Molybdenum foods and flaxseed oil, I developed anemia, insomnia and difficulty tolerating hormone replacement (both thyroid and estradiol).

So far the only relief I get is from Nettle tea. Other copper sources seem to be a bit problematic (oxalates, aromatase inhibition).

The most problematic foods are those high in zinc, iron and vitamin C.

@Mary @picante

 

[Mary]

@Gondwanaland - That's really interesting how the nettle tea is helping you. I just looked up "copper insomnia" and most references say that high copper causes insomnia, e.g., http://holisticpharmd.com/2013/07/04/why-do-you-have-insomnia/ - so I'm wondering how the nettle tea helps with your insomnia. Any ideas?

 

[Gondwanaland]

Any ideas?

I find that copper is a very misunderstood mineral because it is often unavailable in the body, so it will cause symptoms being both high and low. From the site I trust (I highlighted my current issues):

Copper Synergists:
Calcium, potassium, iron, Vitamin E.

Copper Antagonists / Inhibitors:
Sulfur, molybdenum, zinc, nickel, chromium, tin,
Vitamin B6, Vitamin C, hesperidin, insoluble fiber.

Low Levels / Deficiency - Symptoms and/or Risk Factors:

Copper:
Anemia, increased susceptibility for infections,
weakened immune system, hormonal disorders,
increased risk for (colon) cancer, miscarriage,
trabecular bone loss, inflammatory joint disease,
premature graying of hair / loss of hair color,
vascular degeneration, insomnia, stroke, irregular
heart beat (arrhythmia), weight loss, leukopenia,
nerve degeneration, cardiomyopathy (in rats).

High levels / Overdose / Toxicity / Negative Side Effects - Symptoms and/or Risk Factors:

Copper:
Wilson's disease, anemia, nausea, vomiting,
abdominal pain, moodiness, violent behavior,
ADD / ADHD, depression, confusion, weight gain,
hemangiomas,
arthritis, joint / spinal degeneration, higher risk for
some cancers, vascular degeneration (aneurysm,
bruising, hemorrhoids, varicose veins), increased
susceptibility for infections, heart disease & stroke.

Copper Sources:
Wheat germ, oats, fish / shellfish, mushrooms, tea,
soybeans, seeds, coffee, cocoa products, liver, nuts,
drinking water (copper plumbing), copper IUDs.

 

[Gondwanaland]

I would like to add that I personally noticed taking T3 seems to disrupt proper utilization of copper and selenium.
Same for having low estradiol/being on HRT re copper.

 

[Gondwanaland]

So far the only relief I get is from Nettle tea. Other copper sources seem to be a bit problematic (oxalates, aromatase inhibition).

A more careful search is showing me that Nettle is high in iron rather than copper

 

[picante]

A more careful search is showing me that Nettle is high in iron rather than copper

I just looked up Nigella sativa (black seed), and it contains copper. Maybe you could try that:

Besides copper, vitamin C and omega-6 fatty acids, black seed oil contains other nutrients, including vitamin A, vegetable proteins, iron, calcium, thiamin, zinc, niacin, copper, phosphorus and riboflavin.
https://www.livestrong.com/article/29498-black-seed-oil-used/

I started taking black seed oil to break up biofilms. I even swish with it, since dental plaque is a biofilm.

 

[picante]

I find that copper is a very misunderstood mineral because it is often unavailable in the body, so it will cause symptoms being both high and low.

I'm remembering a well-attended discussion on B2 and its ability to release copper from the liver. Do you remember that, Izzy?

 

[picante]

The more I read about the importance of B2, and sufficient thyroxine to activate it, ...

When I first heard about this, I went looking to see whether it has to be thyroxine. I've observed a bias in medical research: they tend to use thyroxine for all these thyroid hormone experiments, and the question is never raised whether T3 will do the same thing.
My searches were pretty fruitless, except a couple bits I saved in my info of B2:

Synthesis of FMN and FAD appears to be influenced by endproduct inhibition and hormones including ACTH, aldosterone, and the thyroid hormones, all of which accelerate the conversion of riboflavin into its coenzyme forms, apparently by increasing the activity of flavokinase.
Advanced Nutrition and Human Metabolism by Sareen Gropper & Jack Smith

In addition, thyroid hormones increase the conversion of FMN to FAD by augmenting the converting enzyme, FAD pyrophosphorylase. Conversely, in hypothyroid states decreased formation of the riboflavin coenzymes FMN and FAD occurs, which produces a hepatic coenzyme profile that mimics true riboflavin deficiency.

[...] Erythrocyte glutathione reductase, an FAD-dependent enzyme, can be used to define riboflavin nutriture. In hypothyroid humans, erythrocyte glutathione reductase activity is reduced. T4 therapy results in normal levels of this enzyme, demonstrating that thyroid hormone regulates the enzymatic conversion of riboflavin to its active coenzyme forms in the human adult.
Kenneth L. Becker
Principles and Practice of Human Endocrinology

 

[CFS_for_19_years]

The more I read about the importance of B2, and sufficient thyroxine to activate it, the more I wonder what happens for those of us who take exogenous T3 and have suppressed T4 levels?

My T4 levels are usually at a trace amount. I have tried switching to NDT, and even tried going mostly off of T3 meds to let my T4 levels come up. Even when I was on a minimal T3 dose (12 mcg per day) my T4 level stayed suppressed. When I took NDT, my body never seemed to take up the T4 and use it.

In both cases, I developed a very hypothyroid state and had to go back on straight T3. My NMH issues go crazy when I get low on thyroid hormones and my brain fog reaches dangerously ditzy levels. My NDT trial ended when I drove the wrong way down a street, thinking it was a 1 way street.

If I am taking one of the Source Naturals active B2 tablets, is this enough to compensate for the lack of thyroxine? Do the regular B2 supplements do anything useful if T4 is low? Is there anything else helpful that can be done?

Thanks!
Michelle

I rely mostly on T3, but I decided to add a small amount of T4 in the form of Armour thyroid after reading the following article:

https://www.ncbi.nlm.nih.gov/pubmed/3809170
Riboflavin metabolism in the hypothyroid human adult

It had been shown that thyroxine regulates the conversion of riboflavin to riboflavin mononucleotide and flavin adenine dinucleotide (FAD) in laboratory animals. In the hypothyroid rat, the flavin adenine dinucleotide level of the liver decreases to levels observed in riboflavin deficiency. We have shown that in six hypothyroid human adults, the activity of erythrocyte glutathione reductase, an accessible FAD-containing enzyme, is decreased to levels observed during riboflavin deficiency. Thyroxine therapy resulted in normal levels of this enzyme while the subjects were on a controlled dietary regimen. This demonstrates that thyroid hormone regulates the enzymatic conversion of riboflavin to its active coenzyme forms in the human adult.

I take the following:
7.5mcg Cytomel every day
one-half of a 15mg Armour tablet once every FOUR days. This is equivalent to 1.125mcg T3 plus 12.5mcg T4

T4 has a much longer half-life than T3, about 7 days, so in my case with this small dose, it works out OK.

 

[picante]

But this study actually looked at the T3/T4 ratios, along with organic acids and all three forms of B2 (riboflavin, FMN and FAD).

Well, this shows how good my memory is . I posted the above in 2015 when I was trying to find out whether T3 will do what T4 does in B2 conversion! Here is the quote I posted:

Riboflavin is the precursor of FMN and FAD, which are implicated in energy metabolism and electron transfer pathways. The conversion of riboflavin into FMN and FAD is catalyzed by riboflavin kinase and FMN adenylyltransferase (EC 2.7.7.2) in the presence of ATP and Zn2+ (30). T3 enhances riboflavin kinase activity (10, 13). The low T3 concentrations observed in PEM might be responsible for a reduction in riboflavin kinase activity, which would give rise to an insufficient conversion of riboflavin into its cofactors. Zinc deficiency, which was described previously in severely malnourished children (31, 32), might also be implicated in the impairment of riboflavin conversion into its cofactors. Along with the thyroid hormone concentrations observed in groups S and C, estimation of energy and zinc intakes in severely malnourished children (group S) and moderately malnourished children (group C) might help explain the observed riboflavin concentrations in group S.
Concentrations of riboflavin and related organic acids in children with protein-energy malnutrition

Note: PEM = Protein-energy malnutrition
Note: Zn2+ is a cofactor!
Note: in the presence of ATP (Gaaaaah , maybe that's what's limiting our conversion.)

 

[Misfit Toy]

I believe T4 is necessary unlike what we are taught. I would love to take it, if I didn't break out in massive rashes from it, have migraines from it. It by far is the worst thing I have ever..and I do mean EVER reacted to. Whether NDT, NP, NT, Armour, you name it..thyroxine compounded....never again. I gave up.

There is another guy on a forum I am on right now who is so sick on T4. He is having fevers, chills, sweating, vomiting and his levels are fine. It's funny because everyone is saying, your levels must be off. They are STTM perfect. He just can't handle it. It's sad.

They really need to have HDT. Human desiccated thyroid. We are not met for pigs thyroids or for synthetic thyroid.

I wonder if I could add T2 to T3. I wonder if that would help me.

Since the thyroidectomy, I have lost strength, will, motivation and gone into menopause. Two years ago, TT, and man...I am done.

In case anyone doesn't know, the movie, SICK TO DEATH is being released on FB on January 18th...about hypothyroidism and how it makes you...you guessed it!

 

[Gondwanaland]

I believe T4 is necessary unlike what we are taught.

T4 is indeed highly needed. The best info I found ouut there about it is here
T4’s role in the body http://www.tiredthyroid.com/rt3-6.html
T3 and T4’s role in the brain http://www.tiredthyroid.com/rt3-7.html
For more articles http://www.tiredthyroid.com/

Having said that, 1 week after starting LT4 back in 2014 I had to see a psychiatrist and ask for an anti-depressant, which I was able to ditch when I switched from LT4 to compounded T4+T3.

I can easily tell when my body is low in glutathione: the 1st sign is depression.

So, in my experience, I would say that T3, rather than T4, activates B2.

ETA- back when I didn't take HRT, minute amounts of B2 would make me depressed. I only started tolerating (minute amounts of) B2 after I started T3.

Interestingly taking selenium never helped, unless in a specific balance with copper. I found a supplement claiming to ensure conversion of T4 into T3, but it doesn't contain copper (perhaps it is in the added herbs?)
https://www.bioticsresearch.com/node/1534

 

[picante]

Copper Antagonists / Inhibitors:
Sulfur, molybdenum, zinc, nickel, chromium, tin,
Vitamin B6, Vitamin C, hesperidin, insoluble fiber.

Izzy, in this info you quoted from acu-cell, I just noticed the insoluble fiber.

Cellulose! It's in so many pills. Last year the doc had me try compounded T3 in a slow-release formula. The slow-release agent was a combination of cellulose and MCC (micro-crystalline cellulose). The stuff went through me without releasing the T3, . I actually got more hypo symptoms on it, and a gut-ache.

But it antagonizes copper, too. Who knew?

 

[picante]

So, in my experience, I would say that T3, rather than T4, activates B2.
ETA- back when I didn't take HRT, minute amounts of B2 would make me depressed. I only started tolerating (minute amounts of) B2 after I started T3.

I've suspected this for a long time: that they do the studies using thyroxine, it converts to T3, and that's the cofactor for riboflavin conversion enzymes. I wish scientists would make these distinctions.

 

[Gondwanaland]

I have an alternative explanation to my reactions, and this might account for different effects in other people:

T3 is precursor of sex hormones. One person low or high in estrogen will tolerate T3 accordingly I suppose. Men also have estrogen issues.

I have very low estrogen. So it is probably not a good idea to get off of T3 entirely in my case. T4 is extremely anti-estrogenic.

Estrogen activates proteases and too low estrogen will impair digestion/proteolysis.

Estrogen also raises serotonin.

 

[Gondwanaland]

For me, I have MCAS. So, it totally fires that right up. I have hives from it and horrible itching.

This thread might interest you
http://forums.phoenixrising.me/index.php?threads/copper-dysregulation.53851/