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Cod liver oil. Ray Peat forum.
.....Yes, 90 of clo is ***t but look opp Rosita and read how they process. Or eat liver which is also high in retinol (more Peat friendy)
Can you share you opinion on clo and explain specifically why you want to avoid it? Im aware that most clo is oxidized or rancid. However i trust a few companies that make high auality products.
I thought clo was highly saturated, thats what ive been told from credible sources and cant really value Peats voice any more compared to them.
It is 27% PUFA of which 21% are Omega 3s, the most susceptible to rancidity. So although it isn't as high in total PUFA as sunflower oil it is high in the Omega 3s that Peat believes are terrible.
Ok and what makes it go rancid? Simply reacting with oxygen within the body?
Fats and degeneration
Your right and my brain is seriously not working latly. Im under high stress. I could have just looked it up. My brain uaed to work relativly OK until i did one single dose of lysine. Now im getting worse every day but i wont go more off topic for now.
Sorry to wake up an old thread, but this post is incredibly useful, thank you very much Amazoniac!
Given that there are people who have tookened 4 million IU and survived, there's a great chance that you will as well and without sequels.
- Pharmacokinetics and safety issues of an accidental overdose of 2,000,000 IU of vitamin D3 in two nursing home patients: a case report
"Much less is known about the toxicity of vitamin D3 following a single high oral dose of vitamin D3. In studies using 300,000 IU [9], 540,000 IU [11], and 600,000 IU [12,13] of oral vitamin D3, no adverse effects were noted and plasma calcium levels or urinary calcium excretion did not change, or only slightly increased for a short period of time, with all cases remaining within the physiological range. In contrast to these reassuring data, Sanders et al. [8] found a significant increase in the risk of falls (+15%) and fractures (+26%) in a randomized controlled trial with an annual dose of 500,000 IU vitamin D3 for 3–5 years in older women compared with placebo. Falls and fractures occurred especially within the first 3 months following the annual dose of vitamin D3. In that study, plasma calcium levels and urinary calcium excretion were not measured; however, bearing in mind the former data, it is unlikely that hypercalcemia occurred in the study. These unexpected findings led Rossini et al. [13,25] to investigate dose-dependent short-term effects on bone turnover markers of a single bolus of vitamin D3. A single dose of 600,000 IU of vitamin D3 increased serum C-terminal telopeptide of type 1 collagen and cross-linked N-telopeptide of type 1 collagen significantly at day 1, attained a peak increment greater than 50% at day 3, and subsequently decreased almost back to baseline values at day 90, without statistically significant changes in plasma calcium [13]. Their results indicate that the use of oral megadoses greater than 100,000 IU of vitamin D may be counterproductive and that the safety issues surrounding vitamin D dosing should not be limited to early markers of vitamin D toxicity as plasma hypercalcemia or increased urinary calcium excretion [13,25]. A possible explanation is the fact that the level of 1,25 dihydroxy-vitamin D is regulated much stronger in the endocrine system than in the autocrine system of vitamin D [5]. If the plasma level of calcidiol (the substrate of the autocrine vitamin D system) increases sharply after a loading dose that deviates too much from the maximum physiological daily dose with sunlight (20,000 IU), this might result in toxic intracellular calcitriol levels in the autocrine vitamin D system without toxic circulating calcitriol levels in the endocrine system of vitamin D and without hypercalcemia. If that is the case, we need other markers than hypercalcemia to prove vitamin D toxicity in the autocrine system, such as bone turnover markers [13]. In any case, more studies are needed to evaluate potential adverse effects of high-dose vitamin D treatment on bone metabolism in relation to fracture risk and risk of falls."
It's curious how some members commented that it's fine without knowing if you already had elevated levels before dosing.
Anyway, for people who took a lot of vit D but without reaching hospitalizing doses, I think there are some measures that are used in those dealing with excess calcium from vit D owadosing that can be useful to implement. The metabolism can remain disturbed for a few months, so a comprehensive test panel is adviseable (Star, 2019). Considerations while one waits for the results..
- Keep calcium intake below 400 mg. At least this is the usual suggested limit, I suppose they've arrived at it through monitoring. If you go extremely low on calcium you might signal the need for releasing calcium from bones and complicate the situation.
- Remain hydrated with liquids that don't provide much calcium. Since excreting excess calcium will be a priority to the kidneys, this alone can cause electrolyte adnormalities, and when you add the extra liquid to the story, it's made worse. The diet should provide plenty of those minerals to avoid this.
- Minimize exposure to oxalic acid to ease the kidney burden.
- It's worth being careful with alkalinizing or acidifying salts because they might have undesirable effects.*
- Magnesium multiple times a day, the forms in this case matter for the reason above, you might worsen the situation with carbonate for example, perhaps glycinate is the best option here.
- Vit K: I would take some k1 and leave mk-4 under the armed pits for the day.
- Vit C is involved in vit D metabolism, so its needs will be increased. There are reports of people who too much of both at the same time and had kidney issues, it's rare but it's something to keep in mind that can happen.
- Taurine is a regulator of calcium in cells.
- Vitamins A and E must be detrimental if you got to a stage where you had to mobilize calcium from bones due to its clearance from circulation with the massive vit D dose (the doses required for this are usually extreme). Vitamin E will cooperate with it and with both you run the risk of increasing your vit K requirements further in an inopportune moment. Otherwise they might be protective.
- Getting plenty of B-vitamins should help in energizing the body to handle rebalancing with class. They're probably depleted with excess vit D.
- 'Lithium hypercalcemia': not sure about the relevance of this.
- Boron: have some doubts if it's beneficial or detrimental here. It might lengthen the duration of the elevated levels of vit D.
- Calcitonin: I has to read more about it.
*Calcium (Dave and Becky)
"Calcium circulates in the ECF in three distinct fractions: about 50% is the biologically important ionised fraction, 40% is protein-bound and is not filterable by the kidney, and 10% is complexed to anions such as bicarbonate, citrate, sulphate, phosphate, and lactate. Most of the protein-bound calcium is bound to albumin, the remainder being complexed to globulins."
"Acidaemia will decrease protein binding and increase the ionised calcium.[8] For each 0·1 decrease in pH ionised calcium rises by about 0·05 mmol/L."
"Several general principles apply to the management of a hypocalcaemic patient. The magnesium level should be checked and, if low, corrected. In a setting of sepsis or renal failure, metabolic acidosis may accompany hypocalcaemia and calcium must be replaced before the acidosis is corrected. Calcium and hydrogen ions compete for protein-binding sites so an increase in pH with alkali therapy will increase the binding sites for calcium, leading to a rapid fall in ionised calcium, potentially resulting in cardiac arrest—unless the calcium is corrected first. Sodium bicarbonate and calcium salts must be infused in separate lines to avoid precipitation of calcium carbonate."
I don't know what to think of phosphate in this story yet. Hyperparatyphoidism makes you excrete phosphate, and the opposite happens from paratyphoid hormone suppression due to excess vit D. Raj has commented about the risk of elevated PTH leading to generalized calcification, but when this first case occurs it presents as high calcium and low phosphorus, which makes it confusing why he suggested that people have been ignored the involvement of phosphate in calcification.
Vitamin A breaks bone down and vitamin D builds up, so when they is in balance the concerted action leads to normal remodeling through the action of osteoclasts and osteoblasts.
Bisphosphonates inhibit the action of osteoclasts on the surface of bone and prevent calcium from being released in massive amounts, which is one of the concerns here. They is phosphate analogs and I don't know if phosphate itself has a similar but weaker action, (from what I read) these analogs are tougher to be acted upon by the phosphate enzymes and this makes them have a lasting effect in preventing the liberation of too much calcium.
And then to complicate it we have the effect of niacin on lowering phosphate.
..
Well, it isn't poisonous, you might feel quite funny in your stomach, but if you take vitamin A and k2 mk4, it should help, but dude, you don't need to take that much at all, even if it isn't fatal, you have no reason to take that much, 50000 ius are max if you want to optimise vitamin D
Agreed. This tidbit almost subtlety escaped, but I caught it on rereading:
