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The Crossover between Hypothyroidism and CFS

frozenborderline

Senior Member
Messages
4,405
http://lesswrong.com/lw/nhs/the_thyroid_madness_two_apparently_contradictory/

This is an odd article, written on the rationalist forum/site lesswrong, which I don't always like as a community. But this comes across as a really important article, tying together cfs and hypothyroid conditions.

I hate when people try and tie cfs into their grand theory, but hypothyroidism is possibly a tricky to diagnose issue, and the medical establishment very well may be wrong about it. I've seen broda barnes' work dismissed as quackery but I've literally never seen any secondary lit that discusses why he was wrong. This article discusses in great detail the conditions of thyroid hormone resistance that mean that your blood tests could show up normal and still you effectively have hypothyroid.

see also: http://lesswrong.com/lw/nbm/thyroid_hormones_chronic_fatigue_and_fibromyalgia/
and :
http://lesswrong.com/lw/n8u/a_medical_mystery_thyroid_hormones_chronic/




sorry if my post is scattered. I'm trying to do too much, it's above my activity threshold rn.

But I think other people may have a field day with looking through these writings. These aren't primary studies, but are writings by someone in the rationalist community proposing a theory of hypothyroidism that explains many chronic illness states

@Hip @Learner1 @pattismith @necessary8 think you all may be interested
 

Sundancer

Senior Member
Messages
569
Location
Holland
thanks @debored13 , I'm not up to reading much yet but will bookmark.

I did read your first link though, and it was decidedly ' enlightening'...

Recently I've been comparing bloodwork done. I saw thyroidtest done in 2005 and had to think, what triggered my GP to test thyroid at that time..ah yeah, i was becoming fat, was not able to get rid of the fat and being fat is just not how I am. Also sluggish in the morning.

Now I realize that the thinning of the brows at that time was already firmly in place. Reading the link, yes, I've struggled with major depression and did ( and do) have IBS.

Now GP is testing for anti-autobodies because blood-work points to hyperactive thyroid.
reading that Myhill says thyroid is the " pushing factor" for mito...oh well...what a shit this is.

Put the puzzle is getting laid, piece by piece.
 

pattismith

Senior Member
Messages
3,931
@debored13 ,

I agree with John Lawrence and Dr Holtorf, the theory and the evidences are strong.

http://forums.phoenixrising.me/index.php?threads/cfs-me-and-intracellular-hypothyroidism.57031/

Thyroid hormons resistance would make a good clinical model for CFS/ME.

My Low T3 syndrome (which is supposed to be a body danger response to different conditions) is also a good clinical model for CFS/ME.

Like you I am looking for a possible link between the danger cell response and a possible thyroid hormons resistance, but cannot solve the equation for now.

Thank you for posting on that exciting subject!
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
 

Attachments

  • Holtorf Thyroid-Hormone-Conversion-Impact-on-TSH-Holtorf-J-Restorative-Medicine-2014.pdf
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  • Holtorf Thyroid-Hormone-Conversion-Impact-on-TSH-Holtorf-J-Restorative-Medicine-2014.pdf
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Messages
90
My experience that is when free T3 is raised to optimal, my SHBG increases (has been as high as 195). This then affects free testosterone adversely which makes me feel bad. My gut feeling is that my body wants me in hypo metabolic state for some reason and messing with these downstream hormones, for me at least, is counter productive.
 

Sundancer

Senior Member
Messages
569
Location
Holland
seeing some people here who are much wiser in thyroid things than I am.

Bloodwork gave B6 way to high ( 511), I did take a Bcomplex with 10mg B6, stopped that now.
I suppose that this has relation with B12 shortage, but that too is a topic that i need to study more.

I wonder whether those high B6 blood-levels can be the reason that my thyroid seems to go in overdrive
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
B6 is used in several processes, like sphingolipid production, heme production, the methionine cycle with B12, and glutathione production.

If you're high in it, it might be because you're missing cofactors for it in one of these processes, so it can't be optimally used.

What kind of test showed it was high? Serum, RBC, ??
 

Sundancer

Senior Member
Messages
569
Location
Holland
just normal bloodtest, ( meaning I dunno ;))
I think the reason that it is so high because of B12 problem. I asked him to test folate too, probably too high too for the same reason.
 

frozenborderline

Senior Member
Messages
4,405
this is quite a lot of info. i'll dive in, soon.

I didn't mean to offend anyone with an idea that CFS is just a thyroid problem.

I'm just trying to figure out thyroid stuff myself. supplementing t3 seems like a big step to take and I want to know what side of the controversy I land on.

I wouldn't think that thyroid stuff is necessarily the cause of CFS but the thyroid is controlled by/related to purinergic signalling, so it could still fit into @necessary8 's theory
 

frozenborderline

Senior Member
Messages
4,405
if titrated properly do you think there is any need to home monitor Bp while doing it or should measuring heart rate and temp be enough
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
I can es feel when I'm on too much T3. I run warm and sweaty, am starving, heart is pounding in my chest.

I got tired of my doctors telling me what to take and seeing labs with FT3 and FT4 at the bottom of the range. I played around with my doses of T4 and T3 until I didn't feel hypo or hyper (realize I've been on thyroid hormones for 7 years, so I knew what I felt like). I finally settled on 137mcg T4 and 50mcg T3 (taken in 2 25mcg doses).

Then I had my labs run and FT3 and FT4 were about 40% from the bottom of the normal range. :)
 

frozenborderline

Senior Member
Messages
4,405
I think my FT3 and FT4 were actually near the top of the range, but TSH was around 1.7 . friend ran values through a new software designed to look at thyroid homeostasis and said i possibly had thyroid hormone resistance
 

frozenborderline

Senior Member
Messages
4,405
"Is there any way that the hypothyroid theory could fit with Naviaux's idea that CFS is a hypometabolic state caused by an issue with purinergic signalling? is there a connection between purinergic signalling and the thyroid? Are there less toxic ways than suramin to "fix" this problem with purinergic signalling?" --me, email to ray peat



ray's response:
"Hypothyroidism is the main factor that causes cell leakiness. Low vitamin E, hypoglycemia, high estrogen, and other things interact. Extracellular ATP is a sign of the damage resulting from low energy producton, the problem that needs fixing is much more basic. "
 

frozenborderline

Senior Member
Messages
4,405
New research is demonstrating that thyroid hormone transport across cellular membranes plays an important role in intracellular triiodothyronine (T3) levels of peripheral and pituitary tissues and is proving to have considerable clinical significance. Reduced T4 and T3 transport into the cells in peripheral tissues is seen with a wide range of common conditions, including insulin resistance, diabetes, depression, bipolar disorder, hyperlipidemia, chronic fatigue syndrome, fibromyalgia, neurodegenerative diseases, migraines, stress, anxiety, chronic dieting and aging, while the intracellular T3 level in the pituitary often remains unaffected. The pituitary has different transporters than every other tissue in the body. The thyroid transporters in the body are very energy dependent and are affected by numerous conditions, including low energy states, toxins and mitochondrial dysfunction, while the pituitary remains unaffected. Because the pituitary remains largely unaffected and is able to maintain intracellular T3 levels while the rest of the body suffers from significantly reduced intracellular T3 levels, there is no elevation in thyroid-stimulating hormone (TSH) despite the presence of wide-spread tissue hypothyroidism, making the TSH and other standard blood tests a poor marker to determine the presence or absence of hypothyroidism. Because the T4 transporter is more energy dependent than the transporter for T3, it is also not surprising that T4 preparations are generally ineffective in the presence of such conditions, while T3 replacement is shown to be beneficial. Thus, if a patient with a normal TSH presents with signs or symptoms consistent with hypothyroidism, which may include low basal body temperature, fatigue, weight gain, depression, cold extremities, muscle aches, headaches, decreased libido, weakness, cold intolerance, water retention, slow reflex relaxation phase or PMS, a combination of both clinical and laboratory assessment, which may include a T3/reverse T3 ratio and the level of sex hormone binding globulin (SHBG), should be used to determine the likely overall thyroid status and if a therapeutic trail of straight T3 or a T4/T3 combination is indicated and not based solely on standard thyroid function tests.
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
Extracellular ATP does a lot of things;

https://www.google.com/url?q=https:...wBNgQFggjMAc&usg=AOvVaw1Ycya0KORxoU-b6altNt9W

Overall conclusions of this thesis are:
i. Substantial literature evidence indicates that ATP and adenosine are extracellular signaling molecules which play a role in the regulation of immunity and inflammation by modulating various immune cell functions;

ii. ATP is likely to play a role in intestinal defence by affecting intestinal permeability on the one hand 9and enterocyte-driven cytokine production on the other hand;

iii. Adenosine seems to exert immunomodulatory effects on human enterocytes, but its precise role


https://www.ncbi.nlm.nih.gov/m/pubmed/22948816/
Abstract
Mast cells are known effector cells in allergic and inflammatory diseases, but their precise roles in intestinal inflammation remain unknown. Here we show that activation of mast cells in intestinal inflammation is mediated by ATP-reactive P2X7 purinoceptors. We find an increase in the numbers of mast cells expressing P2X7 purinoceptors in the colons of mice with colitis and of patients with Crohn's disease.

Treatment of mice with a P2X7 purinoceptor-specific antibody inhibits mast cell activation and subsequent intestinal inflammation. Similarly, intestinal inflammation is ameliorated in mast cell-deficient Kit(W-sh/W-sh) mice, and reconstitution with wild-type, but not P2x7(-/-) mast cells results in susceptibility to inflammation. ATP-P2X7 purinoceptor-mediated activation of mast cells not only induces inflammatory cytokines, but also chemokines and leukotrienes, to recruit neutrophils and subsequently exacerbate intestinal inflammation.

These findings reveal the role of P2X7 purinoceptor-mediated mast cell activation in both the initiation and exacerbation of intestinal inflammation.
 

JES

Senior Member
Messages
1,320
The problem, if it does exist, is likely to be extremely widespread, and explain far more than the mystery of Chronic Fatigue Syndrome and Fibromyalgia. I immediately claim Major Depressive Disorder and Irritable Bowel Syndrome as alternative labels for: 'type II hypothyroidism'. There is a large cluster of these diseases, all mysterious, all with very similar symptoms, known as the 'central sensitivity syndromes'.

The problem I have with his article (that attempts to be scientific) is when I read sentences like this. Essentially he tries to lump CFS, IBS and depression (and probably everything else that doesn't have well established diagnostic markers) into one disease, which he claims is hypothyroidism. This is nothing much different from what the BPS crowd is doing at the moment, where they try to label all these diseases as MUS (medically unexplained symptoms). Or what homeopathy or many other bogus alternative treatments are claiming, that they essentially can treat any disease and every disease is due to "problem X". Just because a disease is not easy to objectively diagnose, it shouldn't be subject to quackery like lumping everything into one category.