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Testosterone and Vitamin D lab results .
Quote from Oliver on April 25, 2021, 8:21 amQuote from tim on March 30, 2021, 6:46 pmBoth sunlight and smoking deplete vit A and carotenoids. Smoking depletes vit A like nothing else, on my YT channel I cover some evidence for that. Vitamin A breakdown products formed from sunlight or smoking are toxic and carcinogenic but if you are poisoned with vit A or Accutane you may create more harm by not depleting retinoic acid as fast as possible. Sunlight exposure is more natural than smoking but this is the first time in human history we have not been exposed to smoke. Cooking food produces many carcinogens and is unnatural too. I've been careful to avoid telling people to smoke. I personally smoke one Manitou organic cigarette per day, don't start smoking half a pack a day...
It's easy to ridicule this idea just as it's easy for low information people to ridicule a low vA diet because it goes against commonly accepted dogma.
Hi Tim, I'm quite interested in this could you please link to your YouTube channel? I've been wondering recently whether it actually depletes VA or simply decreases serum levels by encouraging liver storage
Hi Oliver,
https://www.youtube.com/channel/UCkFhr6r8lvZbGF6UEe9IwIw
Smoke significantly decreases both serum and liver levels.
I've never been of the position that vitamin A is not a vitamin, it's fine if people want to work on some hypothesis and try to refute all the science showing it is but it should never be adopted as a belief to live by. VAD, although extremely rare in rich countries can cause serious harm too. However, Hypervitaminosis A is a common under recognized condition that causes serious systemic harm, it's similar to having taken Accutane.
Do you think that smoke exposure from one or two organic cigarettes per day is more harmful than Hypervitaminosis A? Ask any Accutane user here if they think that Accutane or smoking is harder on the body. Carotenoid and retinoid breakdown products are indeed toxic but ATRA is a teratogenic hormone like signalling molecule and causes incredible harm in excess even more so than excess vitamin D, excess DHT or excess thyroid hormone. So it's obviously important to get retinoic levels down to normal as soon as one can.
I just want to reiterate this as well: I've never told people to smoke, I've just explained why I see it as helpful.
Quote from joshz on May 1, 2021, 5:53 pmdo you feel that smoking has helped your healing? I am curious as a Tobaquero
Hi Josh,
I personally feel it is helpful. Lowering retinoic acid levels is a long process so it's hard to judge objectively.
When you look at the symptom list for Hypervitaminosis A and considering tobacco smoke depletes vitamin A significantly do you see any connection to what you were taught as to what conditions tobacco smoking can help with?
Excessive A is bad on multiple layers, not just for its toxicity. One thing it appears to block vitamin D hormone pathways, replacing calcitriol as a weak VDR agonist(maybe that's the main reason milk contains A but almost no D). People consistently overdo even RDA recommendation for A(counting with all precursors/replacements) which already seems too inflated for all vitamins, not just A based on the outdated/deprecated knowledge of the vitamins roles in human bodies.
All-trans Retinoic Acid Antagonizes the Action of Calciferol and Its Active Metabolite, 1,25-Dihydroxycholecalciferol, in Rats
https://academic.oup.com/jn/article/135/7/1647/4663843
An antagonistic interaction between retinol and calciferol has been established. However, the mechanism by which this antagonism occurs is unclear. One possibility is that retinol affects the metabolism of calciferol. To investigate this hypothesis, retinol- and calciferol-depleted rats were given various amounts of ergocalciferol, cholecalciferol, 1α,25-dihydroxycholecalciferol [1,25(OH)2D3], or 24,24-difluoro-1α,25-dihydroxycholecalciferol [24-F2-1,25(OH)2D3] in combination with various amounts of retinyl acetate or all-trans retinoic acid (ATRA) in a series of studies. Rats administered 1720 or 3440 μg retinyl acetate once every 3 d for 33 d in combination with 25.8 ng ergocalciferol or 25 ng cholecalciferol every 3 d had lower serum calcium and greater serum phosphorus concentrations than rats fed 0 or 11.4 μg retinyl acetate every 3 d. In addition, rats fed 400 μg ATRA/d in combination with 25.8 ng ergocalciferol every 3 d, 25 ng cholecalciferol every 3 d, 2–5 ng 1,25(OH)2D3/d, or 0.5–1 ng 24-F2-1,25(OH)2D3/d had significantly lower serum calcium and higher serum phosphorus concentrations than rats not given ATRA in the diet. Therefore, both retinyl acetate and ATRA are able to antagonize the action of ergocalciferol and cholecalciferol in vivo. Additionally, ATRA antagonizes the in vivo action of 1,25(OH)2D3 and an analog, 24-F2-1,25(OH)2D3, that cannot be 24-hydroxylated. Together, these results suggest that retinol does not antagonize the action of calciferol by altering the metabolism of calciferol or 1,25(OH)2D3, but does so by another mechanism.
...
Although an antagonistic relation between retinol and calciferol has been firmly established, the exact nature of this interaction has yet to be determined. Several studies indicated that retinol may affect the metabolism of calciferol (13,14). Retinol may either decrease the production of the active form of calciferol, 1,25(OH)2D3, or it may increase the destruction of this compound. Another possible mechanism of interaction is that retinol may affect the production of the vitamin D receptor (VDR) (15,16). However, this effect is not clearly established and may depend on species and cell type. A third possible mechanism is suggested by the fact that both all-trans retinoic acid (ATRA) and 1,25(OH)2D3, the active forms of retinol and calciferol, require the retinoid X receptor (RXR) to carry out their effects on gene transcription (17–19). Both ATRA and 1,25(OH)2D3 accomplish their biological functions by binding to specific receptors, retinoic acid receptor (RAR) and VDR, respectively (20,21). These proteins form heterodimers with RXR before binding to specific response elements in the promoter region of ATRA- and 1,25(OH)2D3-regulated genes (22,23). Hence, ATRA or 9-cis retinoic acid (9CRA), the ligand for RXR, may have some effect on 1,25(OH)2D3-induced gene expression. In fact, an RXR-specific ligand, LG100268, was shown to stimulate a calciferol-regulated gene, cytochrome P450 (CYP)24 (24).
Therefore, although an antagonistic interaction between retinol and calciferol has been established in vivo, there is no clear explanation of how this antagonism occurs. The purpose of this study was to investigate the interaction between the 2 vitamins and to gain a better understanding of the mechanism behind it.
Vitamin A antagonizes calcium response to vitamin D in man
https://pubmed.ncbi.nlm.nih.gov/11585356/
For unknown reasons, the highest incidence of osteoporosis is found in northern Europe. In these populations, the sunlight exposure is limited and the vitamin A intake is high. The interaction between vitamin A and D has been the subject of several in vitro and animal studies. We have studied the acute effects of vitamin A and D on calcium homeostasis in 9 healthy human subjects. We compared the effect of (i) 15 mg of retinyl palmitate, (ii) 2 microg of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], (iii) 15 mg of retinyl palmitate plus 2 microg of 1,25(OH)2D3, and (iv) placebo in a double-blind crossover study. The subjects took vitamin preparations at 10:00 p.m. and the following day blood samples were collected five times from 8:00 a.m. to 4:00 p.m. Serum levels of 1,25(OH)2D3 and retinyl esters increased (1.7-fold and 8.3-fold, respectively; p < 0.01). As expected, serum calcium (S-calcium) increased (2.3%; p < 0.01) and S-parathyroid hormone (PTH) decreased (-32%; p < 0.05) after 1,25(OH)2D3 intake. In contrast, retinyl palmitate intake resulted in a significant decrease in S-calcium when taken alone (-1.0%; p < 0.05) and diminished the calcium response to 1,25(OH)2D3 after the combined intake (1.4%; p < 0.01). S-PTH was unaffected by retinyl palmitate. No significant changes in serum levels of the degradation product of C-telopeptide of type I collagen (CrossLaps), or U-calcium/creatinine levels were found.
In conclusion, an intake of vitamin A corresponding to about one serving of liver antagonizes the rapid intestinal calcium response to physiological levels of vitamin D in man.
I think if you become addicted to nicotine that would out-weigh any benefit? (in my opinion)
If you start inching up from your one ciggie a day to two, to three... etc
My small addictions are already a monkey on my back, LOL.
"Do you think that smoke exposure from one or two organic cigarettes per day is more harmful than Hypervitaminosis A? Ask any Accutane user here if they think that Accutane or smoking is harder on the body. Carotenoid and retinoid breakdown products are indeed toxic but ATRA is a teratogenic hormone like signalling molecule and causes incredible harm in excess even more so than excess vitamin D, excess DHT or excess thyroid hormone. So it's obviously important to get retinoic levels down to normal as soon as one can."
With Accutane, is it the inability of the body to eliminate Vitamin A from the liver that's the bigger problem, or the mobilization of Vitamin A from peripheral tissues to get it to the liver? Seems to me that it's the elimination from the liver that is holding everything up (due to excess Vitamin A storage and/or deficiency in detox pathways). If that is the case, then actively mobilizing more retinoic acid from the peripheral tissues via oxidative stress is probably going to cause more injury because there's already a pile-up in the liver...isn't that why that Vitamin A is still stored in the peripheral tissues?
So, it's not a question of whether Accutane or smoking is harder on the body, it's a question of whether Accutane followed by smoking is harder on the body than the effects of Accutane by itself. If you were not yet Vitamin A toxic, and you started taking Accutane, then I think you could make an argument that smoking would hasten the clearance of Accutane from the tissues, which would then be efficiently eliminated by a liver that is not already bogged down. Of course, wouldn't that process also completely defeat the purpose of Accutane? Not that I think Accutane is beneficial, but then you'd just be doubling up on drugs for absolutely nothing!
With Accutane, is it the inability of the body to eliminate Vitamin A from the liver that's the bigger problem, or the mobilization of Vitamin A from peripheral tissues to get it to the liver? Seems to me that it's the elimination from the liver that is holding everything up (due to excess Vitamin A storage and/or deficiency in detox pathways). If that is the case, then actively mobilizing more retinoic acid from the peripheral tissues via oxidative stress is probably going to cause more injury because there's already a pile-up in the liver...isn't that why that Vitamin A is still stored in the peripheral tissues?
Accutane is a megadose of one of the metabolites of vitamin A. Because many people that take Accutane are in a hypervitaminotic state as well they can benefit from a low vit A diet because that will reduce further 13-cis-retinoic acid production over time. This allows 13-cis from the Accutane dose to be cleared more easily. You're likely introducing a strawman that the mechanism by which smoking reduces vitamin A is due to general oxidative stress. It's likely specific chemicals in the smoke that deplete vitamin A. A liver can be full of retinol while tissues can be high in retinoic acid. Smoking depletes both. Retinoic acid outside the liver is the problem and that creates most of the symptoms, when it is metabolized and no longer functions as a hormone it is a lot less problematic.
So, it's not a question of whether Accutane or smoking is harder on the body, it's a question of whether Accutane followed by smoking is harder on the body than the effects of Accutane by itself. If you were not yet Vitamin A toxic, and you started taking Accutane, then I think you could make an argument that smoking would hasten the clearance of Accutane from the tissues, which would then be efficiently eliminated by a liver that is not already bogged down. Of course, wouldn't that process also completely defeat the purpose of Accutane? Not that I think Accutane is beneficial, but then you'd just be doubling up on drugs for absolutely nothing!
Oh mate, you're debating little subtleties of language. It's a question of if smoking is harder on the body than having Hypervitaminosis A for longer and having more exposure to retinoic acid. I think that reducing the time one is exposed to elevated levels of retinoic acid is more important than worrying about exposure to the smoke of a couple of cigarettes per day. It often takes years to deplete retinoic acid levels and studies show that smoking can very quickly deplete retinoic acid levels.
Is there research showing that smoking depletes retinoic acid in people that have Vitamin A toxicity?
How do the chemicals in smoke deplete Vitamin A, and which chemicals? What is the mechanism if it is not oxidative stress of some kind?
Quoted text and citations please.
If I've learned anything in my career as a research biologist who's published peer-reviewed manuscripts, clarity and precision of language is of the utmost importance. I'm not debating subtleties of language, nor am I creating a strawman argument. I'm attempting to clarify your imprecise use of language and identify the assumptions you're making.
Benzo(a)pyrene is the primary constituent of smoke thought to deplete vitamin A. There is animal research showing smoke's vitamin A depleting effect which I cover and cite on my YT channel.
You're not clarifying, you're demonstrating that you don't understand the subject of vitamin A and human health and haven't read through most of this forum, gone through the Ray Peat forum, looked at my YT channel or Garrett Smith's YT channel. Some of us have been studying every aspect of the issue for years now. When I first found out about vitamin A being problematic I didn't start debating others with little understanding, I read Grant's books and then read through every post here and every post on the Ray Peat forum. I then did months of my own research reading studies. Please go and study the basics of vitamin A metabolism. Have you even heard of Anthony Mawson? That's the first thing you need to do, go and read his work. I've posted dozens of referenced quotes on this forum, many of them are key to understanding the subject. Check them out and then come back here and discuss any questions that you have with us.