Conditional problems with vitamin A: a place for sane discussions
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Vitamin A increases SCD1 7x. That alone is reason to take it easy
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Thank you for this. I wonder if i would get banned for posting this in ray peat forum now.
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@Verdad I doubt it. None of the people left there would even understand half of what A. wrote.
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@Kvothe He has terrific word play, Calcium = Kilcium, love that Guy
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@Not_James_Bond we all do
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You guys should look into the RXR. Its a very interesting nuclear receptor.
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@Kvothe I would not be surprised he seems to be basically banning anyone who disagrees with him. He sounds like a deranged cult leader i think it will not be long till he bans anyone posting anything that goes against his theories.
Soon it will be if you post a positive study about Vitamin A or calcium it will be a banning ofense.
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On niacin for NAD
Nicotinamide is now regarded as toxic and nicotinic acid is being favored. It's supplemented intending to increase the synthesis of NAD to detoxify poisons.
They're not using pharmacological amounts of niacin that would lead to marked differences in how each form is eliminated. The moderate doses in use should be readily converted to nicotinamide. This is how forms are metabolized in mice:
The Management of Nicotinamide and Nicotinic Acid in the Mouse
DPN = NAD
desDPN = NaAD (immediate precursor to NAD)
↳ 'des' here stands for 'desamidated' NAD.
Nicotinamide as yield happens with nicotinamide riboside or mononucleotide too:
"NR and NMN were administered by i.v. bolus or oral gavage at 50 mg/kg, which is equivalent to 290 mg in a 70-kg human on a body surface area basis, in the range of common nutraceuticals."
"Unlike in cell culture, where NR and NMN are readily incorporated into NAD (Ratajczak et al., 2016; Frederick et al., 2016), oral administration fails to deliver NR or NMN to tissues without breaking the nicotinamide-ribose bond."
"Irrespective of the route of delivery, the main circulating product of the administered NR or NMN was NAM, which increased by ~20⨯ within 5 min of i.v. NR or NMN; oral NR or NMN administration led to a more modest rise in circulating NAM (Figure 7C)."
I wonder how they justify their aversion to nicotinamide in moderate doses.
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@thyroidchor27 said in Conditional problems with vitamin A: a place for sane discussions:
Vitamin A increases SCD1 7x. That alone is reason to take it easy
Retinoic acids levels are kept relatively stable. What are the conditions for it to occur?
Guys, it was member 'schultz' who started the kill- term trend.
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@Amazoniac in the plasma or in the liver????
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They pride themselves on the fact that it's possible to put psoriasis into remission through poison A deprivation, but what about Coimbra's experiment who accomplished the same with "vitamin" D3 (875 mcg/d) and minor dietary modifications?
These approaches work, but are rudimentary. They manipulate upstream processes rather favoring targeting downstream specifics, that minimize the risk of having to compromise other functions to reach the therapeutic dose (for low or for high).
Psoriasis and beyond: targeting the IL-17 pathway | Nature
Even though targeting what's downstream is more sophisticated, the best thing to do is to try to address the pathogen above it all.
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@thyroidchor27 said in Conditional problems with vitamin A: a place for sane discussions:
@Amazoniac in the plasma or in the liver????
That claim is based on what?
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By the way, you can find various reports of 'undetectable' vitamin D levels; some because of analysis error (it can be challenging to quantify toxins that occur in modest amounts), but others not.
Controlling the availability of the precursor molecule can be a means to make up for an overactive pathway:
Undetectable serum calcidiol: not everything that glitters is gold
"Granulomatous hypercalcaemia is particularly sensitive to vitamin D administration even though toxic 25(OH) vitamin D levels are not reached [5]. This has been attributed to avid 25(OH) vitamin D metabolism into 1,25(OH)2 vitamin D by macrophage 1α-hydroxylase. Availability of 25(OH) vitamin D becomes the main regulator of 1,25(OH)2 vitamin D synthesis. Under these circumstances, treatment of vitamin D deficiency will increase the availability of 25(OH) vitamin D and lead to high 1,25(OH)2 vitamin D levels and hypercalcaemia [8, 9]."
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@Amazoniac said in Conditional problems with vitamin A: a place for sane discussions:
They pride themselves on the fact that it's possible to put psoriasis into remission through poison A deprivation, but what about Coimbra's experiment who accomplished the same with "vitamin" D3 (875 mcg/d) and minor dietary modifications?
Have they presented any evidence regarding vitamin A deprivation and psiorasis, except tweets from good guy Garret Smith and the bible?
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@Kvothe, I'm going by trust in the accounts of reliable people.
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@Amazoniac Are there any in that crowd, and have they controlled their conclusions for other variables? The highly restrictive diets they eat exclude a huge lists of potential irritants that might cause auto-immune conditions and symptoms.
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@Kvothe said in Conditional problems with vitamin A: a place for sane discussions:
@Amazoniac Are there any in that crowd, and have they controlled their conclusions for other variables? The highly restrictive diets they eat exclude a huge lists of potential irritants that might cause auto-immune conditions and symptoms.
'Maybe' to both questions. However, the accounts would be founded.
The Effect of Restricted Intake of Carotene and Vitamin A on Psoriasis Vulgaris
The exclusion of other toxins can contribute to the remission, but I don't think that the addition of isolated poisons to their current diets would lead to positive outcomes.
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@Amazoniac Several people have shown me that paper when I asked for evidence that restriction of vitamin A improves psoriasis. I am sceptical. The authors note that most of the improvements and even complete clearing occured as early as 4/16 weeks after the start of the intervention. That's not nearly enough to significantly deplete retinol stores, especially on a diet that was low, but not insignificant in vitamin A, and it points to something more immediate.
Psoriasis is obviously not caused by excess vitamin A. People with psoriasis, in fact, tend to have lower levels of serum and hepatic retinol, and do not consume excess quantities of it. The underlying cause is found in other processes, and disturbances in the local retinol metabolites are an effect but not the cause of the problem. -
@Kvothe, a diet low in poisons leads to remission and returning with the normal diet results in relapse. Their supplementation without a change in diet does the same. Unless we assume that carotene metabolites are interfering with the action of poisonoic acids or it's disturbing the cell after being incorporated in fatty regions, we have to entertain the other options.
It wouldn't take a minimum of a month to notice the first positive effects from the exclusion of other irritants from the diet, but would match the decrease in circulating carotenes.
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Cyclosporine is also an effective treatment for psoriasis. Given the extensive evidence of vitamin A’s role in immune function, I think it is more likely that psoriasis improvement with a depleting diet is a side effect of immune suppression instead of a root cause being discovered.
https://pubmed.ncbi.nlm.nih.gov/11375434
“Vitamin A deficiency impairs innate immunity by impeding normal regeneration of mucosal barriers damaged by infection, and by diminishing the function of neutrophils, macrophages, and natural killer cells. Vitamin A is also required for adaptive immunity and plays a role in the development of T both-helper (Th) cells and B-cells. In particular, vitamin A deficiency diminishes antibody-mediated responses directed by Th2 cells, although some aspects of Th1-mediated immunity are also diminished.”
