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Alcohol and Vitamin A metabolism
I've been pondering things the last few days and this is what my mind came up with.
We know about the ADH and ALDH pathway that is used for both ethanol and retinol. But this is where the similarities end IMO.
ethanol->acetaldehyde->acetate
retinol->retinaldehyde->retinoic acid
In the first example, with alcohol, the body is taking a potent poison and turning into a benign, water soluble compound, acetate.
In the second example, with retinol, the body it taking a relatively stable compound and turning it into a poisonous compound, retinoic acid.
With the conversion of retinol to retinoic acid, I keep asking "why"?
Why would the body take a relatively stable compound like retinol that is routinely stored in the liver and excreted via the urine (RBP) and bile and essentially turn it into Accutane? Why do we think this is the process that we should try to initiate? With ethanol, the body cannot store and sequester it away and wants it gone. It has the ability to reduce it to acetate and does so. But retinol is a much more ideal form of Vitamin A than freaking retinoic acid.
Retinol is alcohol and fat soluble. It can be excreted via the bile or urine. If it is dumped in the bile, a good portion is reabsorbed and the liver receives it again. It can store it in the liver, wrap a RBP around it/send to urine, or redump it into the bile. If retinoic acid is produced, it can't be excreted via the urine. It isn't water soluble. There isn't a binding protein carrier for retinoic acid that I know of. It can only be dumped in the bile. However, the vast majority of retinoic acid in the bile is reabsorbed (oral Accutane) and the liver now can't really do much with it. When ones take Accutane medication, it is absorbed in the intestines and does whatever it does once it is in the bloodstream. Now, why are we wanting to create more retinoic acid from retinol? What is the advantage?
Although the ADH and ALDH system is great for ethanol, it doesn't follow that just because retinol can be sent through the same pathways, that it is ideal to be sent through said pathways. Maybe it is a last resort or a perfect storm. Maybe the liver fills up with retinol and the conversion is a last ditch attempt to save itself and therefore converts retinol to retinoic acid. This may also happen if other factors are at play like low dietary protein (for RBPs) or alcohol/tobacco/drug interactions.
For the average person, high vitamin A intake leads to high retinol stores. We know alcohol strips the liver of retinol. Maybe this happens to prevent increased liver damage. What if chronic fermentation from sugar/carbs increases activation of the ADH and ALDH systems, converting stored retinol down the pathway to retinoic acid? Retinol is alcohol soluble.
Anyways, just some thoughts floating around my head. 😉
Quote from Armin on August 4, 2021, 11:07 pmI've been pondering things the last few days and this is what my mind came up with.
We know about the ADH and ALDH pathway that is used for both ethanol and retinol. But this is where the similarities end IMO.
ethanol->acetaldehyde->acetate
retinol->retinaldehyde->retinoic acid
In the first example, with alcohol, the body is taking a potent poison and turning into a benign, water soluble compound, acetate.
In the second example, with retinol, the body it taking a relatively stable compound and turning it into a poisonous compound, retinoic acid.
With the conversion of retinol to retinoic acid, I keep asking "why"?
Why would the body take a relatively stable compound like retinol that is routinely stored in the liver and excreted via the urine (RBP) and bile and essentially turn it into Accutane? Why do we think this is the process that we should try to initiate? With ethanol, the body cannot store and sequester it away and wants it gone. It has the ability to reduce it to acetate and does so. But retinol is a much more ideal form of Vitamin A than freaking retinoic acid.
Retinol is alcohol and fat soluble. It can be excreted via the bile or urine. If it is dumped in the bile, a good portion is reabsorbed and the liver receives it again. It can store it in the liver, wrap a RBP around it/send to urine, or redump it into the bile. If retinoic acid is produced, it can't be excreted via the urine. It isn't water soluble. There isn't a binding protein carrier for retinoic acid that I know of. It can only be dumped in the bile. However, the vast majority of retinoic acid in the bile is reabsorbed (oral Accutane) and the liver now can't really do much with it. When ones take Accutane medication, it is absorbed in the intestines and does whatever it does once it is in the bloodstream. Now, why are we wanting to create more retinoic acid from retinol? What is the advantage?
Although the ADH and ALDH system is great for ethanol, it doesn't follow that just because retinol can be sent through the same pathways, that it is ideal to be sent through said pathways. Maybe it is a last resort or a perfect storm. Maybe the liver fills up with retinol and the conversion is a last ditch attempt to save itself and therefore converts retinol to retinoic acid. This may also happen if other factors are at play like low dietary protein (for RBPs) or alcohol/tobacco/drug interactions.
For the average person, high vitamin A intake leads to high retinol stores. We know alcohol strips the liver of retinol. Maybe this happens to prevent increased liver damage. What if chronic fermentation from sugar/carbs increases activation of the ADH and ALDH systems, converting stored retinol down the pathway to retinoic acid? Retinol is alcohol soluble.
Anyways, just some thoughts floating around my head.
I also wondered this question. But if you read a researches, you will find that ALDH PROTECTS cells from the harmful effects of retinol. That is, it is a protective system.
Imagine that you have aldh somewhere, let's say in the lungs. Without these cells, retinol would simply accumulate, oxidize and poison the lungs. But with aldh, it will be output. In addition, the final glucuronated metabolites of retinoic acid are not very toxic and they are easy to output . Retinoic acid is just an intermediate stage.
In addition, acetaldehyde is much more toxic than ethanol.
By the way, one of the main goals of chemotherapy is usually ALDH cells. However, when the aldh cells are restored, the body begins to remove VA again, and the cancer appears with renewed vigor. This is often the case. As Rockarolla says, achieving a temporary remission with a subsequent increase in symptoms.
If you have read my thread about tocotrienol... You will find that the Egyptians who consumed a lot of tocotrienols (which literally burn out the ALDH cells) almost did not get cancer. But they had very common atherosclerosis, which is caused directly by circulating retinol (because they could not remove it). Рhis is the answer to the question of what will happen if the ALDH cells are suppressed. As I said, different VA metabolites create different problems.
Quote from Даниил on August 5, 2021, 4:27 amQuote from Armin on August 4, 2021, 11:07 pmI've been pondering things the last few days and this is what my mind came up with.
We know about the ADH and ALDH pathway that is used for both ethanol and retinol. But this is where the similarities end IMO.
ethanol->acetaldehyde->acetate
retinol->retinaldehyde->retinoic acid
In the first example, with alcohol, the body is taking a potent poison and turning into a benign, water soluble compound, acetate.
In the second example, with retinol, the body it taking a relatively stable compound and turning it into a poisonous compound, retinoic acid.
With the conversion of retinol to retinoic acid, I keep asking "why"?
Why would the body take a relatively stable compound like retinol that is routinely stored in the liver and excreted via the urine (RBP) and bile and essentially turn it into Accutane? Why do we think this is the process that we should try to initiate? With ethanol, the body cannot store and sequester it away and wants it gone. It has the ability to reduce it to acetate and does so. But retinol is a much more ideal form of Vitamin A than freaking retinoic acid.
Retinol is alcohol and fat soluble. It can be excreted via the bile or urine. If it is dumped in the bile, a good portion is reabsorbed and the liver receives it again. It can store it in the liver, wrap a RBP around it/send to urine, or redump it into the bile. If retinoic acid is produced, it can't be excreted via the urine. It isn't water soluble. There isn't a binding protein carrier for retinoic acid that I know of. It can only be dumped in the bile. However, the vast majority of retinoic acid in the bile is reabsorbed (oral Accutane) and the liver now can't really do much with it. When ones take Accutane medication, it is absorbed in the intestines and does whatever it does once it is in the bloodstream. Now, why are we wanting to create more retinoic acid from retinol? What is the advantage?
Although the ADH and ALDH system is great for ethanol, it doesn't follow that just because retinol can be sent through the same pathways, that it is ideal to be sent through said pathways. Maybe it is a last resort or a perfect storm. Maybe the liver fills up with retinol and the conversion is a last ditch attempt to save itself and therefore converts retinol to retinoic acid. This may also happen if other factors are at play like low dietary protein (for RBPs) or alcohol/tobacco/drug interactions.
For the average person, high vitamin A intake leads to high retinol stores. We know alcohol strips the liver of retinol. Maybe this happens to prevent increased liver damage. What if chronic fermentation from sugar/carbs increases activation of the ADH and ALDH systems, converting stored retinol down the pathway to retinoic acid? Retinol is alcohol soluble.
Anyways, just some thoughts floating around my head.
I also wondered this question. But if you read a researches, you will find that ALDH PROTECTS cells from the harmful effects of retinol. That is, it is a protective system.
Imagine that you have aldh somewhere, let's say in the lungs. Without these cells, retinol would simply accumulate, oxidize and poison the lungs. But with aldh, it will be output. In addition, the final glucuronated metabolites of retinoic acid are not very toxic and they are easy to output . Retinoic acid is just an intermediate stage.
In addition, acetaldehyde is much more toxic than ethanol.
Interesting. I've been trying to find what retinoic acid turns into and couldn't find anything until you mentioned glucuronated. Retinoyl-beta-glucuronide seems to be that compound. I may have to research this later. Thanks for the info. 🙂
Watch Garrett Smith's video today and he brought up citrus fruits being really bad. In the video he mentioned how grapefruit and oranges slow down the liver. But from the studies we have listed, lemons actually did the opposite. The delineating factor between grapefruit/orange and lemons may be the vitamin A content.
Lemons have 14 UA
Oranges have 216 UA
Grapefruit has 14,015 UA
Quote from Armin on August 13, 2021, 11:39 amWatch Garrett Smith's video today and he brought up citrus fruits being really bad. In the video he mentioned how grapefruit and oranges slow down the liver. But from the studies we have listed, lemons actually did the opposite. The delineating factor between grapefruit/orange and lemons may be the vitamin A content.
Lemons have 14 UA
Oranges have 216 UA
Grapefruit has 14,15 UA
I wonder what he means by the slow down liver? Does he show any research? If someone knows, I would be grateful if you share it.
Quote from Даниил on August 13, 2021, 12:24 pmQuote from Armin on August 13, 2021, 11:39 amWatch Garrett Smith's video today and he brought up citrus fruits being really bad. In the video he mentioned how grapefruit and oranges slow down the liver. But from the studies we have listed, lemons actually did the opposite. The delineating factor between grapefruit/orange and lemons may be the vitamin A content.
Lemons have 14 UA
Oranges have 216 UA
Grapefruit has 14,15 UA
I wonder what he means by the slow down liver? Does he show any research? If someone knows, I would be grateful if you share it.
He mentioned that grapefruits interact with medications by slowing down the metabolism of the medications, via enzyme interaction. No surprise here.
He referenced a study about raw orange consumption and increased non-alcoholic-fatty-liver-disease. I believe it may be due to fructose primarily or in combo with vitamin A.
Quote from Armin on August 13, 2021, 12:58 pmQuote from Даниил on August 13, 2021, 12:24 pmQuote from Armin on August 13, 2021, 11:39 amWatch Garrett Smith's video today and he brought up citrus fruits being really bad. In the video he mentioned how grapefruit and oranges slow down the liver. But from the studies we have listed, lemons actually did the opposite. The delineating factor between grapefruit/orange and lemons may be the vitamin A content.
Lemons have 14 UA
Oranges have 216 UA
Grapefruit has 14,15 UA
I wonder what he means by the slow down liver? Does he show any research? If someone knows, I would be grateful if you share it.
He mentioned that grapefruits interact with medications by slowing down the metabolism of the medications, via enzyme interaction. He referenced a study about raw orange consumption and increased non-alcoholic-fatty-liver-disease.
https://econtent.hogrefe.com/doi/pdf/10.1024/0300-9831/a000292
I wonder what kind of "other fruits" were here, I don't have access to a full study. But apparently, this is either fructose, or soluble fiber (which Garrett loves so much), or VA, not citrus.
http://www.whfoods.com/genpage.php?tname=foodspice&dbid=25
Also grapefruit contains a ton of lycopene.
I've noticed over time that I like beer NOT to be hoppy. Hoppy beers are so "in". Some of them taste EXACTLY like grapefruit juice. ew.
I've noticed something about the plant world. Plant toxins show up in more than one plant. Some herbs smell exactly like lemon: lemon balm, lemon basil and others. They invented aspirin from willow trees, but the active ingredient is present in other things (saycylates). Almond flavor is present in several things.
I wouldn't be surprised if beers--so heavily hopped that they taste like grapefruit juice-- have some of the other qualities of grapefruit juice too.