Chris Masterjohn: Salicylates are Toxic
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@CrumblingCookie said in Chris Masterjohn: Salicylates are Toxic:
Elevated 1,25-OH-D3 binds into thyroid receptor alpha simulating high thyroid levels when they aren't.
Trying to decode. I suppose this means: that high vitamin D can influence thyroid function by reducing the number of thyroid hormone receptors (TR), which can indirectly mimic some effects of hypothyroidism by decreasing overall thyroid hormone action.
=> HD vit D3 supplement takes the place / occupies thyroid hormone receptors.
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@LucH
No, it's different. 1,25-OH-D3 displaces T3 as the native ligand from its binding to thyroid receptor alpha which casts both peripheral thyroid hormone action as well as the feedback mechanisms into disregulation. 1,25-OH-D3 is not meant to be a circulatory but a predominantly paracrine hormone. The serum measurings of it are for the most part essentially a gradient-dependent reflection of intracellular levels. Cranking up D3 and 25-OH-D3 forces pathologically high 1,25-OH-D3 concentrations even higher because these hormones exert opposite metabolic action. The D3 supplementation debate is a masterpiece of mind-fuckery and gatekeeping to trap and blind the populace in meaningless busy-work as to why everyone's health is going to shits. -
@CrumblingCookie
So, if I try to make it clear (with the help of ChatGPT). Thanks by advance, if I miss sth. I know it exhausts energy ...
Question to ChatGPT:- Need an oversimplification, not an explanation from why and how.
- What does it imply if corrected formulated?
Highlight:
“Too much vitamin D can blur the body’s thyroid ‘messages,’ even if thyroid hormone itself is normal.”
Explanation (oversimplified if I did it well)
See it as a mini cause-effect chain, stripped down to essentials:- High vitamin D intake → raises active vitamin D (1,25-OH-D3) in the cells if ...
- Active vitamin D → binds to thyroid receptors (VDR) and pushes thyroid hormone (T3) aside.
- Result: Thyroid signals don’t work as they should in the body.
- Extra result: The brain also gets confused about thyroid levels (since the feedback loop is disrupted).
- Outcome: You can show thyroid-like symptoms or test results without actually having a true thyroid hormone problem.
Edit: See also
Vitamin D Receptor stops mitochondria respiration [Why vit D can cause problems] [1,25 vitamin D]
https://bioenergetic.forum/topic/2433/vitamin-d-receptor-stops-mitochondria-respiration-why-vit-d-can-cause-problems-1-25-vitamin-d
NB: You'll need aspirin afterwards. -
@LucH The LLM / "AI" is making mistakes:
"Active vitamin D → binds to thyroid receptors (
VDRTRalpha and TRbeta)"but otherwise it covered the gist of it.
Point 5. actually raises attention to the next possible fallacy from this context: Spending one's lifetime trialling and discussing thyroid hormone dosing schemes instead of D3, or even both, in a ceaseless effort to mitigate symptoms.
Good find of late Travis's lookings into this. It's hard to read and was sadly left unrefined in its many implications. I much appreciacte @cs3000's posts but, without pressuring anyone into believing anything, he was wrong about making these deductions:
@cs3000 said:So by this, need to fix thyroid before you can tolerate vitamin D well preventing excessive conversion to 1,25 and not having so much around that inhibits an already impaired mitochondria. and also need to lower macrophages if they're elevated (chronic inflammation) as they raise this 1,25 vitamin D form and inhibit mitochondria too.
That just raises the absurdity and reciprocity of running after an ever-eluding carrot. The answer's not in such running about like a headless chicken within the transgressing deceptions to entangle scientific, public and individual discourse but in inquiring the causes of and reasons for why the ratio of 1,25-OH-D3 to 25-OH-D3/24,25-OH-D3/D3 is out of whack and why macrophages are chronically overactive in the first place. Why is iron low and sequestrated and hepcidin high. That's really all I would have to say about this. Keep up your energy.
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@CrumblingCookie Is this true in every case though, i.e. that supplementing 25-OH-D3 leads to (pathologically) high calcitriol levels?
I know that in sarcoidosis and other similar such diseases, supplementing with D3 is bad because it will just cause macrophages to produce a bunch of calcitriol.
But in healthy people, taking 25-OH-D3 should (at least in theory) lower PTH levels which then reduces the synthesis of calcitriol in the kidneys. So in the short-term vitamin D3 increases calcitriol, but in the long-term it lowers PTH/calcitriol.
I am myself conflicted on the issue whether vitamin D is good or bad.
I avoided it strictly for many years due to the logic behind the Marshall protocol, but honestly, it hasn't been that helpful and I think I just got vitamin D and calcium deficient (translucent teeth and other calcium deficiency symptoms). So I think I was wrong and Ray peat was right. Obviously getting it from the sun is best but there is no sun where I live 9 months out of 12
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@Korven said:
But in healthy people, taking 25-OH-D3 should (at least in theory) lower PTH levels which then reduces the synthesis of calcitriol in the kidneys. So in the short-term vitamin D3 increases calcitriol, but in the long-term it lowers PTH/calcitriol.
I don't see that that's how it works. It suppresses PTH but not calcitriol synthesis. What happens is that the D3 and 25-OH exceedingly overwhelm the body's conversion capacities so that their concentrations (antagonists) outcompete the 1,25-OH (agonist) in VDR (but not thyroid etc. receptors) binding. Ray was hesitant in his late years to adapt a more particularized view on the matter. Marshall and associated researchers likely held back (were made to restrain?) further thoughts and implications beyond an VDR agonist mechanism and beside that the medical assocations regained a firm grip on the latter's temporary word of mouth and prescribing. As an adequate subsitute for light, sunlight, UV- and IR-spectra exposure D3 also utterly fails as the former serve far more and different physiological functions. It's another misleading narrative and false premise. Really the whole thing is kind of like a dishonest discussion on the best dosing regimen and bioavailibities of dexamethasone against one's inflammated lungs and breathing impairments without ever looking for or even caring about pulmonary TB or an asbestos environment. Or discussing the ideal continuous application forms of ibuprofen or diclofenac against somebody's pelvic pains while neglecting any UTI background. It's from the tricksters' playbook.
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@CrumblingCookie Hm interesting... thanks for the reply.
I know Trevor Marshall has said in one of his lectures that there is no such thing as a vitamin D deficiency, only a calcium deficiency. Do you believe that is accurate?
After avoiding vitamin D supplementation for a couple of years (only sun exposure and going to tanning beds) my levels have been hovering around 17-18 ng/ml. Recently I started taking 5000 IUs oral vitamin D to see if it would help with my slightly translucent teeth and neck stiffness.
Not sure but I feel like my teeth are looking a little more solid, and I also feel like it has helped with energy levels. But it also makes me feel extremely lethargic and stupid, like a cortisol crushing feeling, so I've stopped taking it for now.
The hype around vitamin D3 supplements feels like a psy-op, but who knows...
I think I will just have to move to Spain or something
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@LucH Much appreciated!
I've been away for several days and need to read through all of your provided notes.
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@CrumblingCookie
I appreciate the alternative view. I'll consider what you say and weigh it against against the various perspectives. Thank you. -
@Korven said in Chris Masterjohn: Salicylates are Toxic:
I know Trevor Marshall has said in one of his lectures that there is no such thing as a vitamin D deficiency, only a calcium deficiency.
And yet another perspective, from the RPF, some years back where I was corresponding with someone who felt:
"Basically, I think a vitamin D deficiency is indicative that you a) may have excess calcium and your body is trying desperately to avoid absorbing more..."
Interesting and challenging to have all these perspectives.
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@Mossy said in Chris Masterjohn: Salicylates are Toxic:
I appreciate the alternative view.
I'm trying to connect the dots between active vit D3, what could be seen as an excessive take, VDR enzyme blocked and defensive mechanism and poor liver metabolism...
Vitamin D, Calcium and mineral metabolism with Dr. Ray Peat and Kate Deering. Jun 23, 2021
From Winatlife Podcast transcript
Dr. Peat uses the references of 25OHD /hydroxycholecalciferol (stored) and 1,25D (active).
https://www.youtube.com/watch?v=ur9F7THGBLg (Possibilité d’afficher la transcription pdt l’interview). 1.46’As a reminder Vitamin D has many names
The three most mentioned in this podcast are
Cholecalciferol [or calciferol] also known as D3 (what is in food, fish oil, or supplements).
"Stored D" also known as calcidiol / 25OHD /hydroxycholecalciferol
"Active D" also known as calcitriol / 1,25DIn this episode we talk about…
The purpose of Vitamin D.
How is vitamin D metabolized and stored.
How much D is too much?
The difference between Active and Stored Vitamin D.
Can "stored D" have active properties?
Is elevated Active D (1,25D) a good thing?
Do Vitamin D supplements suppress the immune system?
The Vitamin D "receptor" theory-is it correct?
Are blood levels of stored D (25OHD) correct?
What are optimal stored Vitamin D levels?
The relationship between D and Ca.
Understanding the importance of parathyroid hormone (PTH).
What can affect PTH besides Calcium and Vitamin D.
What causes calcified tissue.
Understanding the calcium -magnesium connection.
What ratios, if any, are optimal for minerals?
Understanding Hair Tissue Mineral Analysis? Are they accurate?NB: I've got the script version. Still Trying to connect the dots. I'll do it with RP & CM, to avoid mismatch. Personal opinion. Need time. For an advanced state comprehension.
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@Korven said:
that there is no such thing as a vitamin D deficiency, only a calcium deficiency. Do you believe that is accurate?
Yes. Regular small amounts of calcium. Boron also plays along with that through a variety of mechanisms incl. hormones, aluminum and renal mineral retention. Potassium is a big factor for the latter as well and by itself boosting magnesium sufficiency. And menatetrenon K2 mk4 is noticably powerful.
@LucH said:
pdf transcript link
Ray talked about it between minutes 35-46. By the sound of it Kitty was rather a little befuddled and disappointed wrt his replies. I certainly am. It was a half-informed and condescending rant that sticks out from this more commonly applied modesty. He was all into anti-inflammatory arguing that non-inflammated cells and tissues were strong and resilient enough to withstand irritants. There's a good core belief in it but as one follows it round the circle it's incongruent and nonsensical. His concept of immunity was that it increases inflammation and that's bad and for the old and sick (...). I fear you won't be able to connect the dots from that.
indeed.
I dare say could Travis have followed this up he would have delivered a coherently explained and backed-up piece of work. -
@CrumblingCookie said in Chris Masterjohn: Salicylates are Toxic:
I dare say could Travis have followed this up he would have delivered a coherently explained and backed-up piece of work.
Thanks for your input and the warning (inflammation). I appreciate. I'll try to find Travis post on old RP forum, though I have to proceed indirectly. I no longer go there if I can avoid it
No need t explain why, I think.
Bye.
