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The Concealed Causes of "Thyroid Resistance"

Discussion in 'Thyroid Dysfunction' started by drob31, Sep 24, 2014.

  1. drob31

    drob31 Senior Member

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    I was reading through a post by Cigana which is about 3 years old and it got me thinking about hypothyroid symptoms and how they manifest even when numbers are in range and all blood work comes back normal. In this post, I'm not going to focus on obvious causes, like high estrogen, high TBG, or RT3. Although RT3 does show a metabolic down regulation consistent with high levels of cortisol.

    The two people I consistently keep coming back to on this issue are Chris Kresser, and David J Clark.

    Chris Kresser has authored a number of insightful articles about hypothyroid conditions. Of particular interest is his detailed article about how adrenal issues cause hypothyroid symptoms.


    ADRENALS

    In this article he lists 5 ways in which the adrenals will cause hypothyroidism. The first two directly lower t3, but since we're assuming numbers are at least in the normal range, will throw those out. Number 3 addresses the auto immune factor, so we'll throw that out too, however we'll come back to autoimmune, because it's possible you have an autoimmune condition without testing positive for any antibodies.

    "4) Adrenal stress causes thyroid hormone resistance
    In order for thyroid hormone circulating in blood to have a physiological effect, it must first activate receptors on cells. Inflammatory cytokines have been shown to suppress thyroid receptor site sensitivity.

    If you’re familiar with insulin resistance, where the cells gradually lose their sensitivity to insulin, this is a similar pattern. It’s as if the thyroid hormone is knocking on the cell’s door, but the cells don’t answer.

    While there’s no practical way to measure receptor site sensitivity in a clinical setting, the research above suggests it is decreased in autoimmune and other inflammatory conditions. A perfect example of this in practice is the Hashimoto’s patient who is taking replacement hormones but still suffers from hypothyroid symptoms – often in spite of repeated changes in the dose and type of medication. In these patients, inflammation is depressing thyroid receptor site sensitivity and producing hypothyroid symptoms, even though lab markers like TSH, T4 and T3 may be normal."

    But the $64,000 question, is: What's causing the adrenal dysfunction? Let's throw out the notion that they get "fatigued." They are doing what they are told, and something is telling them to do that. You figure out the cause of this, and you fix everything, if you can treat it.


    "Balancing the adrenals
    Here’s the tricky thing about adrenal stress: it’s almost always caused – at least in part – by something else. These causes include anemia, blood sugar swings, gut inflammation, food intolerances (especially gluten), essential fatty acid deficiencies, environmental toxins, and of course, chronic emotional and psychological stress."


    High cortisol causes T3 receptors to shutdown. You can have super physiological amounts of t3 floating around from taking high doses of cytomel, but it has no affect because it can't dock with the receptor:




    AUTO IMMUNE

    Most are familar with Hashimoto's, and we're assuming you did not test positive for the antibodies. However, that doesn't mean you don't have Hashimoto's. Say what?

    According to David J Clark:

    "You're lucky if you were tested and you actually showed elevated antibodies. Scientific research shows that about 15 percent of Hashimoto's victims are seronegative---they don't make enough antibodies to be detected. Even though they really do have Hashimoto's and have got all the symptoms"

    Also,

    You can have positive TSH antibodies for Grave's, but it actually causes Hashitmotos:




    INFLAMATION (Cytokines)

    [​IMG]



    Chris Kresser gives us an example for our adrenals in how cytokines can disrupt the HPA axis, however this event would show up in thyroid blood work, so it doesn't really count: "Studies have shown that the inflammatory cytokines IL-1 beta, IL-6 and TNF-alpha, which are released during the stress response, down-regulate the HPA axis and reduce levels of thyroid stimulating hormone (TSH)."

    However, these same cytokines do something else, which just like as we saw with high levels of cortisol, high levels of cytokines shutdown t3 receptors, and lab numbers look normal.




    HOMOCYSTEINE

    Those with MTHFR should keep an eye on this one. With poor methylation and high homocysteine, you could become hypothyroid, and all your other lab numbers could appear normal.
    "Homocysteine can dock on a cell and have it stop having a response to thyroid hormone."




    VITAMIN A DEFFICIENCY

    This is a bit of an odd ball, but still a potential cause, and not caught on normal blood work labs.




    The one thing that jumps out at me after going through this material is how the adrenal glands can cause hypothyroidism via multiple mechanisms at the same time.

    High cortisol can:

    • Shut down t3 receptors
    • Cause high rt3, which could block receptors that aren't shut down
    • Interfere with pituitary and hypothalamus signaling (lowering TSH)
    • Cause auto immune conditions (Hashimoto's --- you can have it even if you tested negative to antibiodies)
    • HPA-axis disruption causes high cytokines which shutdown t3 receptors (but bloodwork looks normal!)
    • Raises TBG which lowers free t3

    ALL AT THE SAME TIME!
     
    PatJ, Rlman, Mogwai and 2 others like this.
  2. knackers323

    knackers323 Senior Member

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    Very interesting but what is the treatment?

    Higher doses of T3?
     
  3. ukxmrv

    ukxmrv Senior Member

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    But for this to have any relevance to CFS or ME we would need the high cortisol part wouldn't it?

    People with CFS and ME seem to largely low cortisol though.
     
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  4. drob31

    drob31 Senior Member

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    I'm not sure if that would help depending on how badly receptors are being shutdown. The resistance seems to be caused by the thing that needs to be fixed. However, it would make sense that super physiological doses of t3 would overcome this somewhat.
     
  5. cigana

    cigana Senior Member

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    It's all interesting.
    I tried super physiological doses and saw no improvement, personally.
    I have found it hard to verfiy the role played by various substances in blocking receptors - it's difficult to find reliable scientific evidence for this effect (not saying it doesn't happen).
     
  6. Aileen

    Aileen Senior Member

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    would supplementing iodine, rather than the hormones themselves be more beneficial?
     
  7. ahmo

    ahmo Senior Member

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    The first thing that impacted on my then unlabelled illness, after my collapse w/ ME, was getting off the synthroid I'd been taking for decades. I asked a number of MDs for an alternative in that first year, and stayed w/ the GP who agreed. Then there were 5 years working w/ GP and compounding chemist trying various combinations of natural thyroid, T3, T4. When it was finally evident that none of these would work, rT3 levels significant, I began my own research and found John Lowe and his T3 protocol. T3 was, and remains, the thing that works for me.

    I tried super physiological doses of T3 in 2010-11, following John Lowe's protocol. I'd spent many hours reading his info, even purchased his textbook, not wanting to miss any crucial point. And yet, he missed a crucial point. As I understood his protocol, I could expect to experience a relaxation of my nervous system, and if my symptoms did not abate, I should continue raising doses. However, it was only after I eliminated gluten that I got any relief. And there was zero mention of gluten in his huge book.:thumbdown:

    My current experience is that there is a very delicate balance between my adrenals and thyroid. Well, not my thyroid gland, but thyroid medication. My gland is pretty much non-functioning. I had a major detox event in May which quite clearly centered on adrenals. At this point I was on 30mcg T3. As I listened to speakers in the Thyroid Summit, I tried to increase my T3. Didn't work: insomnia, adrenal pain. I took heart in someone in that forum emphasizing to not worry about getting temperature's up. Even when I was on about 120mcg years earlier, I never got up to normal temps.

    Now, 4 months later, things are different. 1) Eliminating gluten cross-reactive and auto-immune stimulating foods. 2) 3 months on low dose naltrexone. 3) No iodine, including no celtic sea salt. (Datis Kharrazian confirms this as necessary for many) 4) Ongoing attention to adrenals through coffee enemas (detox liver to relieve adrenals. Best solution I've found). Since my detox event in May I've no longer needed the adrenal glandulars that I relied on for 2 years.

    I began experiencing weight gain and fluid retention, so began to increase T3. I'm now at 70mcg, and have had normal temps, tho not daily. I'll continue bumping this up, at 10-11 day intervals, per Rudy Dragone, one of the best of the Thyroid Summit speakers. I'll increase until it seems to be the right dose: no hyper or hypo sx. I also just learned to take thyroid rx away from B vits. I'd been taking them together, have only rectified this during this past week. (Datis Kharrazian)

    I'm now, for the first time in my life, not ingesting anything to stimulate antibody reactions. I only learned from Dragone that there was cornstarch in my T3 rx,:bang-head: and switched to compounded. I gave up relying on blood tests for anything following John Lowe's counsel. My GP doesn't even suggest them anymore. But I will request one at my next appt, as I'd like to see what they show.
     
    Last edited: Sep 26, 2014
  8. drob31

    drob31 Senior Member

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    Do you have any thoughts into why your high doses did not override this? Receptors being shutdown?
     
  9. drob31

    drob31 Senior Member

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    I was going to add a low cortisol section, but if cortisol is too low it would prevent t3 from adequately entering the cells.
     
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  10. drob31

    drob31 Senior Member

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    It depends on if you're deficient or not. I would tend to say no, since my personal experience was negative. Iodine was the only thing that started to make me feel almost 100% normal, but then a week later it crashed me back down, even worse. It's bad for Hashimoto's and it can cause hypothyroid symptoms if doses are too high. Some have success with it, however.
     
  11. Gondwanaland

    Gondwanaland Senior Member

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    Right now my goal is some day to be able to supplement iodine.

    I have high antibodies (anti thyroglobulin) and have just started titrating levothroyd up, according to this protocol:
    http://advancingthyroidcare.wordpress.com/2010/03/21/three-phases-of-treating-hashimotos/

    For the 1st time I got a lab result below 800 for the antibodies after 1 month on Levothyroxine. Next week I will see a new dr about T3.

    Then I will consistently supplement the cofactors, selenium, zinc, magnesium, B complex and vit C according to http://www.stopthethyroidmadness.com/2013/12/29/companion-nutrients-the-key-to-iodine-protocol/

    And then iodine. Wish me luck :eek:

    Starting the methylation protocol made me hypothyroid and with a goiter :(

    The energy generation stimulated by mB12 apparently used up my low iodine levels :grumpy:

    izzy
     
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  12. knackers323

    knackers323 Senior Member

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    What is the idea behind seperating B vits and thyroid meds?
     
  13. ahmo

    ahmo Senior Member

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    @knackers323
    Better absorption of thyroid on it's own. So sayeth one of the thyroid experts, I'm pretty sure Kharrazian. I've got a lot of respect from him after hearing his recent presentation.
     
  14. ahmo

    ahmo Senior Member

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  15. drob31

    drob31 Senior Member

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    I'm starting to wonder if some people are having mitochondria dysfunction in the periventricular nucleus in the hypothalamus. This leads to all of the hormonal imbalances, including thyroid and adrenal issues.
     
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  16. Gondwanaland

    Gondwanaland Senior Member

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    picante likes this.
  17. drob31

    drob31 Senior Member

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    That's fascinating, but I must admit, it's a very grey area. I think various forms of mitochondrial disease which occur via mutation sporadically, or from virus or autoimmune probably cause a good portion of CFS issues. I guess it depends which system in the body is affected by the mutation.

    This is something Dr. Myhill writes about extensively:

    Chronic fatigue syndrome is the symptom caused by mitochondrial failure

    The job of mitochondria is to supply energy in the form of ATP (adenosine triphosphate). This is the universal currency of energy. It can be used for all sorts of biochemical jobs from muscle contraction to hormone production. When mitochondria fail, this results in poor supply of ATP, so cells go slow because they do not have the energy supply to function at a normal speed. This means that all bodily functions go slow.

    http://www.drmyhill.co.uk/wiki/CFS_-_The_Central_Cause:_Mitochondrial_Failure
     
  18. Little Bluestem

    Little Bluestem All Good Things Must Come to an End

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    How far apart should they be taken?
     
  19. Mogwai

    Mogwai

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    @drob31

    A very timely piece, thank you.
     
  20. ahmo

    ahmo Senior Member

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    Little Bluestem likes this.

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