ME/CFS stopped with outbreak of autoimmune disease

[Martin aka paused||M.E.]

I am definitely not a "total remission" patient yet (and do not know if I ever will be). But my doctor, in additional to anecdotal reports, said that many people get the maximum benefit at the six month mark, and I am only at the three month mark, so it is still possible for me to have additional improvements, beyond those that I have already had.

I wish you a total remission!

 

[Wishful]

Gingergrrl, one thing you could possibly try is T2 (3-5 diiodothyronine). The T4 and T3 supplementation might have reduced your gland's production of T2. T2 is definitely important in my ME/CFS. I take it once every 21 days, and it seem to 'reset' something (possibly needed for producing proteins). If I forget to take it then, my symptoms increase and stay increased until I remember to take the T2. Iodine (a drop of tincture on bread) works almost as well, but T4 and T3 don't have any such effect. I assume the iodine boost allows the thyroid gland to produce more T2.

It works for me, but I've posted it here before and no one else has posted that it helps them, so I guess it has only a remote chance for helping you. The temporary improvement from T4/T3 which then got worse just makes me suspicious that T2 levels are involved.

I'm also very sensitive to goitergens, such as brassicas. If you feel worse after eating brassicas (especially raw), then it's more likely that you need supplemental T2. People with thyroid problems should probably avoid brassicas anyway.

The product I use is San T2 Xtreme (sold as a fat loss, body building product). The previous version didn't have the 3-3 isomer, but worked just as well.

 

[Gingergrrl]

I wish you a total remission!

Thank you so much @MartinDH and I really hope so too!

The T4 and T3 supplementation might have reduced your gland's production of T2.

I think that Armour Thyroid (the med I take) actually has T2 in it, in addition to T3 and T4.

Iodine (a drop of tincture on bread) works almost as well

I do not do well with iodine at all and my Endo said not to take it.

I'm also very sensitive to goitergens, such as brassicas.

Just Googled "brassicas" and I am okay with all of the veggies that it listed (whatever that may mean)?!

 

[Wishful]

Supplemental iodine works for me, but probably not for some thyroid problems that don't convert the iodine into hormones properly.

As for goitrogens (misspelled it earlier), maybe I have some unusual thyroid dysfunction. A piece of broccoli is enough to make my symptoms worse, and T2 is very effective for me.

While thinking about it, I remembered that the medical exam I had when this whole mess started showed that my thyroid function was fine (though I can't remember if it showed antibodies). Tests years later showed elevated tsh. The immune system dysfunction of ME/CFS might have induced greater thyroid antibody activity. However, I still believe that my elevated tsh is due to elevated kynurenines caused by neuroinflammation. My tsh of 8 or so might be 'normal' for someone suffering from chronic neuroinflammation. Thyroid tests really should take inflammation into account.

 

[Wishful]

Gingergrrl, I did take Armour Thyroid for three months. It didn't do anything for me, so by that it seems that it doesn't have enough T2 to make a difference. I'm not trying to push T2, but just clarifying that Armour Thyroid isn't proof that supplemental T2 doesn't help. It's too bad that T2 testing isn't readily available. If doctors did test for it, they might find that it's actually important to test for.

 

[Gingergrrl]

Gingergrrl, I did take Armour Thyroid for three months. It didn't do anything for me, so by that it seems that it doesn't have enough T2 to make a difference.

I actually don't know for sure and thought my Endo said that it did but would need to clarify. For whatever reason, Armour has worked well for me and my thyroid issues are under control.

 

[Wishful]

I wanted to point out that supplemental T2 does inhibit production of T4 and thus T3, so probably not a good thing to experiment with if you're having problems with those two.

On another note: I think I've evidence that T2 products do get weaker over time. I was feeling worse for the last couple of weeks, and wondering why. It might have been pork (bought ham and pork steaks), or handsawing firewood (triggering PEM). I stopped both for a few days and still felt lousy...as if the T2 I'd taken last time hadn't worked. Then I remembered that usually I take a drop of iodine first, then T2 later in the day or the next day. Last time I skipped the iodine. I took a drop of iodine yesterday, and feel better today. I need a bit longer to make sure that it's not just a random fluctuation, but I think I should buy some fresh T2. The last batch is around four years old...

 

[PracticingAcceptance]

Too brain foggy to take in all the words but I thought I'd say... also interested in this thread.

In addition several people have reported that their ME symptoms improve in pregnancy. This is linked to better immune tolerance to the baby.

So, if I get pregnant, I'll feel better? And maybe if I get ill with colds, I'll feel better? Or psoriasis? So if this theory is right, maybe we could infect ourselves on purpose with something different with less bad symptoms, and have that instead of ME? Would that work?

And maybe a cure could look like an invented infection that doesn't actually have bad symptoms, which takes the place of ME. I'm not a scientist, haha, this is more like going down the dystopian novel route.

Or maybe we could trick our bodies into thinking we're pregnant all the time to give us symptom relief.

 

[Mithriel]

Lots of autoimmune diseases improve during pregnancy, but no on has come up with a treatment that mimics it.

 

[pattismith]

Hi @MartinDH ,

Going back on this switching from Psoriasis to ME and vice versa via a switch in T lymphocytes, I found a recent paper that gives a bit more informations about it:


"Human Tregs appear metabolically flexible, switching between glycolysis-only and both glycolysis and fatty acid oxidation upon activation (36).
In addition to providing energy for cell survival and division, the choice between utilizing glycolytic and oxidative metabolism defines the lineage decision between Th17 cells and Tregs, respectively (13) (reviewed in ref. 37).

The decision to oxidize fatty acids for OXPHOS is taken by Tregs in addition to memory T cells (14) and is influenced by nutrient status, via mTOR and AMPK activation as well as pyruvate dehydrogenase kinase 1 (PDHK1) activation, Acetyl-CoA carboxylase 1 (ACC1) expression (13, 14), and PTEN activity (38, 39)"

So when T cell choose glycolytic metabolism, it matures into Th17 cells (associated with Psoriasis in your case)

and when T cell chose oxidative metabolism, it matures into Treg cells (expressing FOXP3 but with impaired activity which lead to ME)

It seems that Cimetidine (anti acid drug) can do this switch but you have to pay attention to possible side effects, because a trial was done on psoriasis patients and two of them had side effects.

 

[Martin aka paused||M.E.]

Hi @MartinDH ,


It seems that Cimetidine (anti acid drug) can do this switch but you have to pay attention to possible side effects, because a trial was done on psoriasis patients and two of them had side effects.

I don't understand much of what you say but I will give this a look when I'm less brainfogged. Thank you so much for this input!

 

[leokitten]

@MartinDH I’ve had a rare form of psoriasis since my late teens. It was constantly misdiagnosed by doctors for so many years and therefore not treated properly. In my mid 30s before getting ME it started getting worse and then after getting ME it got a lot worse and harder to control. It is definitely in the realm of possibility that my living with the psoriasis untreated for so long caused changes in my body that put me at high risk of getting ME.

I believe there is a definite connection between the two diseases, for me in particular the symptoms of both ME and psoriasis go up and down together (the “flare ups”).

What you said about psoriasis biologics is very true, many patients do not respond well enough to anti-TNF therapy and have seen remission with newer, more targeted anti IL-17 and IL-23 therapies. I believe some of us have said the same about rituximab and ME here on PR, just like with MS many patients don’t respond well to rituximab yet have seen long remissions on newer anti CD-19 biologics. So B-cell targeting might still prove useful even thought the phase III had a negative overall result.

 

[sue1234]

MartinDH,

I didn't see from your original post about coming down with psoriasis, did you take any meds at that time for it? Or did it just come on and then clear up later on its own?

 

[pibee]

My ME started when my Hashimoto started too!

 

[i-lava-u]

This is a very interesting thread. It shows how different all of us are. But my brain hurts seeing the differences

My psoriasis flares up when my ME gets worse.

I also have psoriasis and it always flairs when my ME flairs

And some of us are more genetically prone to making antibodies. In going through my health history, my ME/CFS specialist noted I had Hashimotos, celiac, and multiple food allergies and immediately created an action item to see if I had antibodies that have been noted in ME/CFS patients, which I did.

could u tell me which antibodies you were tested for that have been noted in ME/CFS? never knew this and sounds interesting

In addition several people have reported that their ME symptoms improve in pregnancy. This is linked to better immune tolerance to the baby.

I had the opposite effect, felt worse ME symptoms with pregnancies and had pre-eclampsia with both

It is definitely in the realm of possibility that my living with the psoriasis untreated for so long caused changes in my body that put me at high risk of getting ME.

ME started in 1995 (viral onset) first got psoriasis in 2005 when pregnant with second child.

?!

 

[Martin aka paused||M.E.]

MartinDH,

I didn't see from your original post about coming down with psoriasis, did you take any meds at that time for it? Or did it just come on and then clear up later on its own?

I would say I had it for a year flaring up... then it stopped a year ago. And this summer, my joints were in massive pain for about one month. Then pain went away and bam: ME!

 

[pattismith]

While thinking about it, I remembered that the medical exam I had when this whole mess started showed that my thyroid function was fine (though I can't remember if it showed antibodies). Tests years later showed elevated tsh. The immune system dysfunction of ME/CFS might have induced greater thyroid antibody activity. However, I still believe that my elevated tsh is due to elevated kynurenines caused by neuroinflammation. My tsh of 8 or so might be 'normal' for someone suffering from chronic neuroinflammation. Thyroid tests really should take inflammation into account.

TSH over 10 mIU/l = hypohyroidism but TSH between 5 and 10 = subclinical hypothyroidism, so 8 doesn't seem normal to me...

 

[Wishful]

As I said, 8 might be 'normal' for someone suffering from neuroinflammation. Inflammation increases picolinic acid, which increases MIPS, which increases trh, which increases tsh. I haven't found any direct information about inflammation raising tsh this way, but it is logical, just under-researched.

 

[pattismith]

Hi!

I have been a mild case for many years. Then, two years ago, my psoriasis broke out (for the first time). Right after the beginning of the psoriasis my CFS/ME symptoms stopped. They came back a few months ago (while my psoriasis has gone). Now I'm moderate.

Does anyone have any idea why? I wonder if this is a sign for the condition being linked to the immune system. Kind of a proof?

Thank you all!

Hello Martin, I know you are now very severe and that maybe you won't be able to read my post,
but I wanted to share with you this information that could be the answer to your question.

I found these infos in these scientific articles:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5808178/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1798459/

To sum up, Chlamydia Trachomatis can induce skin lesion that are similar to psoriasis, but the name is different:

keratoderma blenorrhagicum

Myalgic Encephalitis is believed to be linked with activated inflammation with elevated TNF-alpha and activated P2X7 receptors.
By the way both activated P2X7 and TNF-alpha have shown to protect against Chlamydia!

So your ME/CFS may be linked to P2X7 activation and/or TNF-alpha elevation, which immediatly put under control your chlamydia, and makes your skin lesions disappear.

If this is right, treatment to lower these immune activation may help you

 

[S-VV]

Would it then be expected that Chlamydia may downregulate P2X7, and that could explain the temporary improvement?