Orion Log
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what you think of Retin-A? I used to use this for a year before I crashed. Stopped taking it though cause find it sketchy.
Orion
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From what I have read topical is just is bad as oral.
MNK99
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Never really replaced it and was scared to use it, but I had 18-20months or longer of retin A creams. Anti aging creams. I used them when I started ADD meds... nothing happened (nothing bad). -- I did take accutane. DMG? who knows. (serious dmg from Effexor (earlier) and Finasteride (later). I think I could use it fine now. It was expensive, I got some free (medical, cosmetic grade). Surely has some risks (suicidal depression? doubt it but who knows). They say wait till 30. So I barely used it at that time.
I mean I exfoliated my face and used cream with it like twice a day at times. I have ADD so I didn't do it long (ran out, had other shyt to worry about than replacing it).
I mean I exfoliated my face and used cream with it like twice a day at times. I have ADD so I didn't do it long (ran out, had other shyt to worry about than replacing it).
Orion
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So its been about 1 month running no supps after a full ARL mineral cycle, electrolytes, lots of liver flushes, and ended with a 25 day water fast.
Being off cycle I am seeing an increase in shedding and some shinkage, so I does seem with me the zinc/manganese combo does stop shedding completely, did not see regrowth, but stopped hair falling out. Also more blood flow and NO available for libido. Sending in hair sample for TEI in 2 weeks, looking forward to getting a few TEI cycles done this year. Sleep, skin conditions, body comp, and mood are all still doing great.
Being off cycle I am seeing an increase in shedding and some shinkage, so I does seem with me the zinc/manganese combo does stop shedding completely, did not see regrowth, but stopped hair falling out. Also more blood flow and NO available for libido. Sending in hair sample for TEI in 2 weeks, looking forward to getting a few TEI cycles done this year. Sleep, skin conditions, body comp, and mood are all still doing great.
How is your health in terms of the post accutane condition?
Orion
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Everything is heading in a positive direction, and firmly believe mineral balancing stops hairloss.
i think their major source of vit A or rather carotene comes from sweet potato , right !! Beta-carotenes have much less toxicity than Active vitamin A.
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there is no such a thing as active vitamin A/ retinols have metabolism. retonoic acid is active. vit A needs 5 steps at least to become active.
and people claim that A is easily oxidized since it is PUFA. they eat a lot more pufa in their diet , than they would get from supping vitamin A
Beta carotene needs b12 to convert into A. and A needs zinc, NAD moly b2, etc. to get to retinoic acid.
I dont like taking fat soluble vitamins. And I agree with you that beta carotene is better.
since I think if you have b12, only then you should have A in blood.
So I partially agree that A as animal vitamin is not good in excess and I would def never supplement fat solubles too much
I think vitamin A toxicity could put pressure on vitamin B12 and copper .
thus people who have A but lack b12. because of potassium deficiency. lets say.
they would get psoriasis and other things from lack of b12. skin problems, etc.
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Orion
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Posting this here as not sure where as, but some good info on how vitamin A reduces NADPH and glutathione. Those of us you took accutane, it is imperative that we deplete it from our bodies, either very long water fast or zero vitamin A diet. I am now close to 4 months zero vitamin A and it is doing great things. Viewing vitamin A as a un-essentiall and pretty much a toxin is looking more and more real. So if you have PFS and continue to eat or use TEI supps with vitamin A (palmitate - ParaPack), I think you will have trouble progressing. Also roundup(Glyphosate) is in the food chain bigtime, and it blocks the breakdown of vitamin A, and seems to decrease glutathione as well.
Taken from a guest post on Genereaux's blog
======================
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1217027/pdf/8660285.pdf
Retinoic acid modulation of glutathione and cysteine metabolism in chondrocytes(Cartilage)
“Secondly, we found that intracellular glutathione levels are regulated by retinoic acid. Thus, in the presence of physiological concentrations of the retinoid, there is a profound decrease in both glutathione and cysteine levels. It is probable that the concomitant decrease in both cellular and extracellular cysteine concentrations results from the change in intracellular glutathione metabolism.”
(JF: well, duh, - the body uses Cysteine to make Glutathione, so they might want to beef-up that "probable" to a "most likely" and still leave room to be wrong. Let's see; deplete Glutathione with Retinoic Acid, check, put the cells/tissue in a panic to create more, check, the local Retinoic Acid inspired emergency grabs every scrap of Cysteine it can find, check, but where's the Glutathione we might assume the Cysteine was used to make? Is this another one of those - "We may have taken such a short-term look at the situation, that our snapshot doesn't actually represent what's going on, but we're confident we'll eventually get to the bottom of it all"? Did they give the Cysteine a chance to become Glutathione? How did they both disappear? What did they disappear into? Is this some kind of Retinoic Acid-as-Conan scenario, broadsword slicing everything to bits? Remember that paper from 2018 that said if researchers had extended the time-parameters of the studies they performed (it was a review paper), that they might find out Retinoic Acid was the cause of all of the Autoimmune Diseases? I wonder if that review group is still working somewhere? Siberia, perhaps? How’d that line even get past the editorial board? Oh, I forgot already, peer-review takes 4 years.)
(JF: I guess you could say “regulated” (above), but the word doesn’t have the same meaning that most of us are walking around with. It's like saying, “The life of the test animal is regulated by Arsenic”. Then they throw a few more variables into the mix and end with a conclusionary kludge. I wonder what the meaning of "modulating" is to these folks. Could it eventually come to light that "modulating" actually means the body creates Glutathione to protect itself from mad-scientists running around, killing and torturing rodents by the millions, with beakers full of Retinoic Acid in their hands?)
“Finally, we explored the effect of medium components on chondrocyte thiol status. We noted that while ascorbate alone did not change cell thiol levels, (JF: presumably in the cells) it did cause a 4-fold decrease in the extracellular cysteine concentration (JF: that’s interesting for sure). When retinoic acid and ascorbic acid were both present in the medium, there was a marked decrease in the level of glutathione. In contrast, the phosphate concentration of the culture medium served as a powerful modulator of both glutathione and cysteine.
(JF: is "modulator" the same as "regulator"?)
Results of the study clearly showed that there is a profound decrease in intracellular levels of both cysteine and glutathione (JF: due to Retinoic Acid) and that thiol levels are responsive to ascorbic acid and the medium phosphate concentration. These findings point to a critical role for thiols in modulating events linked to chondrocyte maturation and cartilage matrix synthesis and mineralization.”
Thirdly, we noted that caudal chondrocytes contain half as much glutathione as do the cephalic cells and the level of the thiol is not influenced by retinoic acid. The profound differences in thiol metabolism between cephalic and caudal chondrocytes suggest that the retinoid effects are cell specific, possibly related to the acquisition of receptors by cephalic cells.
(JF: now that one looks like a clue. Cell specific retinoic acid effects. Hmmm)
Considering the control of cellular thiol levels, the investigation clearly showed that the retinoid [retinoic acid] caused a dose-dependent decrease in the intracellular concentrations of glutathione and cysteine.
(JF: now we have three words; “regulates”, “modulates”, and “controls”).
Retinoic acid inhibits anaerobic energy metabolism; accordingly, a reduction in glycolysis would limit pentose phosphate shunt activity and lead to a drop in the level of NADPH, a required co-enzyme for glutathione synthesis.
Environ Toxicol Pharmacol. 2007
Cysteine turnover in human cell lines is influenced by glyphosate.
Pesticides are widely spread in the environment and there is a lack of knowledge concerning the impact of these substances on the human cell. In the present study the effect of low doses of the pesticides bentazon, metalaxyl and glyphosate on the cellular metabolism of glutathione and cysteine was examined in HeLa and hepatoma cell cultures. No effect was observed when the cells were exposed to bentazon or metalaxyl. However, significant changes in the intra- and extracellular concentration of cysteine, a precursor for glutathione synthesis, were detected when glyphosate was added to the medium. This finding was observed in the presence of micromolar concentration range of glyphosate, and is relevant when compared to concentrations observed in monitoring programmes.
From Wiki on Cysteine
Precursor to the antioxidant glutathione[edit]
Due to the ability of thiols to undergo redox reactions, cysteine has antioxidant properties. Its antioxidant properties are typically expressed in the tripeptide glutathione, which occurs in humans and other organisms. The systemic availability of oral glutathione (GSH) is negligible; so it must be biosynthesized from its constituent amino acids, cysteine, glycine, and glutamic acid. While glutamic acid is usually sufficient because amino acid nitrogen is recycled through glutamate as an intermediary, dietary cysteine and glycine supplementation can improve synthesis of glutathione[15].
(JF: that’s pretty much what I’m looking for, even as I lob the blue-collar razz at these researchers. (Hey, most of it is our tax dollars anyway, we want our money's worth, eh?) If we know that Retinoic Acid is the main problem in Retinoid Toxicity, and we know that it depletes Glutathione in cells, and that dietary Cysteine and Glycine can help us make Glutathione, then what’s not to like about that? These amino acids may not be direct counters to Retinoic Acid, but they sound like they can be very helpful in a protection sense at the very least, and at levels (cells, organs and tissues) in which we might not perceive the beneficial effects right away. In fact, some things we probably can’t perceive until significant damage is done and pain or something else sneaks up on us. I still think there could be a more direct effect in play, so I’ll keep looking at that angle. The paper about Glycine versus Necrosis is enough to make me think there’s more to it than just a powerful antioxidant effect. There's so much information out there about Glycine, Taurine, Cysteine, and their part in transmembrane proteins (among other things) that it wouldn't surprise me to find something simple in the studies that medical science has ignored for years.)
Taken from a guest post on Genereaux's blog
======================
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1217027/pdf/8660285.pdf
Retinoic acid modulation of glutathione and cysteine metabolism in chondrocytes(Cartilage)
“Secondly, we found that intracellular glutathione levels are regulated by retinoic acid. Thus, in the presence of physiological concentrations of the retinoid, there is a profound decrease in both glutathione and cysteine levels. It is probable that the concomitant decrease in both cellular and extracellular cysteine concentrations results from the change in intracellular glutathione metabolism.”
(JF: well, duh, - the body uses Cysteine to make Glutathione, so they might want to beef-up that "probable" to a "most likely" and still leave room to be wrong. Let's see; deplete Glutathione with Retinoic Acid, check, put the cells/tissue in a panic to create more, check, the local Retinoic Acid inspired emergency grabs every scrap of Cysteine it can find, check, but where's the Glutathione we might assume the Cysteine was used to make? Is this another one of those - "We may have taken such a short-term look at the situation, that our snapshot doesn't actually represent what's going on, but we're confident we'll eventually get to the bottom of it all"? Did they give the Cysteine a chance to become Glutathione? How did they both disappear? What did they disappear into? Is this some kind of Retinoic Acid-as-Conan scenario, broadsword slicing everything to bits? Remember that paper from 2018 that said if researchers had extended the time-parameters of the studies they performed (it was a review paper), that they might find out Retinoic Acid was the cause of all of the Autoimmune Diseases? I wonder if that review group is still working somewhere? Siberia, perhaps? How’d that line even get past the editorial board? Oh, I forgot already, peer-review takes 4 years.)
(JF: I guess you could say “regulated” (above), but the word doesn’t have the same meaning that most of us are walking around with. It's like saying, “The life of the test animal is regulated by Arsenic”. Then they throw a few more variables into the mix and end with a conclusionary kludge. I wonder what the meaning of "modulating" is to these folks. Could it eventually come to light that "modulating" actually means the body creates Glutathione to protect itself from mad-scientists running around, killing and torturing rodents by the millions, with beakers full of Retinoic Acid in their hands?)
“Finally, we explored the effect of medium components on chondrocyte thiol status. We noted that while ascorbate alone did not change cell thiol levels, (JF: presumably in the cells) it did cause a 4-fold decrease in the extracellular cysteine concentration (JF: that’s interesting for sure). When retinoic acid and ascorbic acid were both present in the medium, there was a marked decrease in the level of glutathione. In contrast, the phosphate concentration of the culture medium served as a powerful modulator of both glutathione and cysteine.
(JF: is "modulator" the same as "regulator"?)
Results of the study clearly showed that there is a profound decrease in intracellular levels of both cysteine and glutathione (JF: due to Retinoic Acid) and that thiol levels are responsive to ascorbic acid and the medium phosphate concentration. These findings point to a critical role for thiols in modulating events linked to chondrocyte maturation and cartilage matrix synthesis and mineralization.”
Thirdly, we noted that caudal chondrocytes contain half as much glutathione as do the cephalic cells and the level of the thiol is not influenced by retinoic acid. The profound differences in thiol metabolism between cephalic and caudal chondrocytes suggest that the retinoid effects are cell specific, possibly related to the acquisition of receptors by cephalic cells.
(JF: now that one looks like a clue. Cell specific retinoic acid effects. Hmmm)
Considering the control of cellular thiol levels, the investigation clearly showed that the retinoid [retinoic acid] caused a dose-dependent decrease in the intracellular concentrations of glutathione and cysteine.
(JF: now we have three words; “regulates”, “modulates”, and “controls”).
Retinoic acid inhibits anaerobic energy metabolism; accordingly, a reduction in glycolysis would limit pentose phosphate shunt activity and lead to a drop in the level of NADPH, a required co-enzyme for glutathione synthesis.
Environ Toxicol Pharmacol. 2007
Cysteine turnover in human cell lines is influenced by glyphosate.
Pesticides are widely spread in the environment and there is a lack of knowledge concerning the impact of these substances on the human cell. In the present study the effect of low doses of the pesticides bentazon, metalaxyl and glyphosate on the cellular metabolism of glutathione and cysteine was examined in HeLa and hepatoma cell cultures. No effect was observed when the cells were exposed to bentazon or metalaxyl. However, significant changes in the intra- and extracellular concentration of cysteine, a precursor for glutathione synthesis, were detected when glyphosate was added to the medium. This finding was observed in the presence of micromolar concentration range of glyphosate, and is relevant when compared to concentrations observed in monitoring programmes.
From Wiki on Cysteine
Precursor to the antioxidant glutathione[edit]
Due to the ability of thiols to undergo redox reactions, cysteine has antioxidant properties. Its antioxidant properties are typically expressed in the tripeptide glutathione, which occurs in humans and other organisms. The systemic availability of oral glutathione (GSH) is negligible; so it must be biosynthesized from its constituent amino acids, cysteine, glycine, and glutamic acid. While glutamic acid is usually sufficient because amino acid nitrogen is recycled through glutamate as an intermediary, dietary cysteine and glycine supplementation can improve synthesis of glutathione[15].
(JF: that’s pretty much what I’m looking for, even as I lob the blue-collar razz at these researchers. (Hey, most of it is our tax dollars anyway, we want our money's worth, eh?) If we know that Retinoic Acid is the main problem in Retinoid Toxicity, and we know that it depletes Glutathione in cells, and that dietary Cysteine and Glycine can help us make Glutathione, then what’s not to like about that? These amino acids may not be direct counters to Retinoic Acid, but they sound like they can be very helpful in a protection sense at the very least, and at levels (cells, organs and tissues) in which we might not perceive the beneficial effects right away. In fact, some things we probably can’t perceive until significant damage is done and pain or something else sneaks up on us. I still think there could be a more direct effect in play, so I’ll keep looking at that angle. The paper about Glycine versus Necrosis is enough to make me think there’s more to it than just a powerful antioxidant effect. There's so much information out there about Glycine, Taurine, Cysteine, and their part in transmembrane proteins (among other things) that it wouldn't surprise me to find something simple in the studies that medical science has ignored for years.)
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I dont agree with this about vitamin A
Retinol protects glutathione same as b caroteen, it is A FACT.
Retinoic acid increases metabolism is puts pressure on glutathione. Vitamin A is not retinoic acid and converts to it on needed basis.
you need to understand that to produce retinoic acid body needs b2)) and moly and 5 reactions. only then retinoic acid can increase metabolism )))
Thus retinoic receptor is protected by glutathione. https://www.sciencedirect.com/science/article/pii/S0006291X09019147
So to make retinoic acid you need FAD, so when body makes it )) body knows that there is glutathione.
and stupid accutane bypasses this regulation. and depletes glutathione
and thus later on retinoic metabolism does not work)
same as FIN depleting NADPH and FAD and thus glutathione, accutane does the same
and thus retinoic metabolism stops either on zinc part, or on aldehyde part, which causes symptoms and histamine,
which that guy experienced.( like eczema etc)
(PDF) Retinol but not retinoic acid can enhance the glutathione level, in a manner similar to β-carotene, in a murine cultured macrophage cell line
https://www.sciencedirect.com/science/article/pii/S0041008X14002658
Beta-carotene reduces oxidative stress, improves glutathione metabolism and modifies antioxidant defense systems in lead-exposed workers (Journal Article) | OSTI.GOV
Inhibition of glutathione depletion by retinoic acid and tocopherol protects cultured neurons from staurosporine-induced oxidative stress and apoptosis, Neurochemistry International | DeepDyve
that canadian dude is probably fast oxidizer
Retinol protects glutathione same as b caroteen, it is A FACT.
Retinoic acid increases metabolism is puts pressure on glutathione. Vitamin A is not retinoic acid and converts to it on needed basis.
you need to understand that to produce retinoic acid body needs b2)) and moly and 5 reactions. only then retinoic acid can increase metabolism )))
Thus retinoic receptor is protected by glutathione. https://www.sciencedirect.com/science/article/pii/S0006291X09019147
So to make retinoic acid you need FAD, so when body makes it )) body knows that there is glutathione.
and stupid accutane bypasses this regulation. and depletes glutathione
and thus later on retinoic metabolism does not work)
same as FIN depleting NADPH and FAD and thus glutathione, accutane does the same
and thus retinoic metabolism stops either on zinc part, or on aldehyde part, which causes symptoms and histamine,
which that guy experienced.( like eczema etc)
(PDF) Retinol but not retinoic acid can enhance the glutathione level, in a manner similar to β-carotene, in a murine cultured macrophage cell line
https://www.sciencedirect.com/science/article/pii/S0041008X14002658
Beta-carotene reduces oxidative stress, improves glutathione metabolism and modifies antioxidant defense systems in lead-exposed workers (Journal Article) | OSTI.GOV
Inhibition of glutathione depletion by retinoic acid and tocopherol protects cultured neurons from staurosporine-induced oxidative stress and apoptosis, Neurochemistry International | DeepDyve
that canadian dude is probably fast oxidizer
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@Orion but I agree with you I dont like fat soluble vits
If we look at the livers of animals. they are usually high in what/
high in copper, high in vitamin A and high in iron.
this is because the metabolism is usually slow in people. because of stress.
that is why all vitamin A foods, have potassium with it.
and feeding copper and vitamin A is stupid. if you dont speed up metabolism
SO fasting is viable and good option, and may be carnivour diet for slow oxidizers.
If we look at the livers of animals. they are usually high in what/
high in copper, high in vitamin A and high in iron.
this is because the metabolism is usually slow in people. because of stress.
that is why all vitamin A foods, have potassium with it.
and feeding copper and vitamin A is stupid. if you dont speed up metabolism
SO fasting is viable and good option, and may be carnivour diet for slow oxidizers.
Orion
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Fasting did great things for me for sure. I will keep reporting how the zero vitamin A diet goes, its helping tons. Will definitely give a 6 month and 1 year report.
Still waiting on my newest TEI hairtest, should have it any day now.
Orion
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Lastest TEI results attached - Slow 1
TEI from one year ago: Mar 2018
Aluminum is one one toxic min, and I have used tons of silicic acid, but not moving much, will keep at it.
I just calculate the mineral amount per day and take them, here is my daily main vitamin mineral intake:
B1: 20mg
B3: 125mg
B5: 100mg
B6: 165mg (large, pyroluria)
Biotin: 3.75mg (large, pyroluria, push sugar metabolism)
Folinic acid: 800mcg (instead of meythylfolate)
Zn: 17mg
Mn: 6mg
Se: 250mg
Mg: 600mg
Cr: 1200mg (large, push sugar metabolism)
Vit E 400IU
HCl 1Xmeal
So this leads me to believe that the the algorithms are leaning towards Pyroluria:
"Pyroluria and Heme Synthesis
Remember that pyroluria involves the malfunction of heme-containing molecule degradation and excess production of HPL. Animal studies have shown that excess levels of HPL cause a decrease in liver heme and the heme-containing detoxification enzyme cytochrome P450. It is estimated that this decrease can measure up to 55% (3). Zinc, vitamin B6, and biotin are all required for the production of heme. The loss of these nutrients through pyrrole affinity and excretion creates a major disruption in heme levels. Proper balances of heme are required for many other body functions as well, including oxygen regulation and electron transfer, two very critical homeostatic functions."
TEI from one year ago: Mar 2018
Aluminum is one one toxic min, and I have used tons of silicic acid, but not moving much, will keep at it.
I just calculate the mineral amount per day and take them, here is my daily main vitamin mineral intake:
B1: 20mg
B3: 125mg
B5: 100mg
B6: 165mg (large, pyroluria)
Biotin: 3.75mg (large, pyroluria, push sugar metabolism)
Folinic acid: 800mcg (instead of meythylfolate)
Zn: 17mg
Mn: 6mg
Se: 250mg
Mg: 600mg
Cr: 1200mg (large, push sugar metabolism)
Vit E 400IU
HCl 1Xmeal
So this leads me to believe that the the algorithms are leaning towards Pyroluria:
"Pyroluria and Heme Synthesis
Remember that pyroluria involves the malfunction of heme-containing molecule degradation and excess production of HPL. Animal studies have shown that excess levels of HPL cause a decrease in liver heme and the heme-containing detoxification enzyme cytochrome P450. It is estimated that this decrease can measure up to 55% (3). Zinc, vitamin B6, and biotin are all required for the production of heme. The loss of these nutrients through pyrrole affinity and excretion creates a major disruption in heme levels. Proper balances of heme are required for many other body functions as well, including oxygen regulation and electron transfer, two very critical homeostatic functions."
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Orion
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LOL
Orion
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Its the mega B6 that worries me, but going to test it out. @HerrFisch
HerrFisch
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Was too. Had a similar b6 dosage. But different story/problems. Do you have any experience with b6 supplementation?
You know I meant the mcg/mg right ?
That's cool you're starting your second big round of minerals etc but... It is a mistery why your results didn't stick from your first round of minerals.. You were used to take them for a long time but it didn't stick.
Maybe you should think that you're not kicking the root of the problem... No?