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A theory on enhancing Vitamin A excretion by enhancing glucuronidation
🙂 Actually, yeah, it is a Chris Masterjohn article.
I found the WAPF article you likely read. It is from 2004, so Chris Masterjohn was probably in college way back then! I wonder if he would agree with these views many years later. He also seems to state that the effect of high protein is to move retinol from the liver to other tissues of the body, which is not necessarily a positive outcome if you are focused on getting vitamin A out of your body. Still, it would be great if eating more protein lets you excrete more vitamin A.
For others, the key paragraphs from the article are:
The utilization of protein requires vitamin A. Several animal studies have shown that liver reserves of vitamin A are depleted by a high dietary intake of protein, while vitamin A increases in non-liver tissues. One explanation for this is that adequate protein is necessary for vitamin A transport. In one study researchers fed radioactively-labeled vitamin A to rats on low-protein and high-protein diets, using the amount of radioactivity present in exhaled gases, urine and feces as a measure of the metabolism of vitamin A, and found that vitamin A is indeed used at a higher rate on a high-protein diet.6
Vitamin A is not only depleted by a high intake of protein, but it is also necessary for the synthesis of new protein, which is the goal of the bodybuilder. Rats fed diets deficient in vitamin A synthesize protein at a lower rate than rats fed adequate vitamin A.7 Cultured skeletal muscle cells increase the amount of protein per cell when exposed to vitamin A and D, but not when exposed to vitamin D alone.8
The references are
- Furusho, et. al., “Tissue specific-distribution and metabolism of vitamin A are affected by dietary protein levels in rats,” Int J Vitam Nutr Res. 1998;68(5):287-92
- Narbonne, et. al., “Protein metabolism in vitamin A deficient rats. II. Protein synthesis in striated muscle,” Ann Nutr Aliment. 1978;32(1):59-75.
- Stio, et. al., “Synergistic effect of vitamin D derivatives and retinoids on C2C12 skeletal muscle cells,” IUBMB Life. 2002 Mar;53(3):175-81
https://www.westonaprice.org/health-topics/vitamin-a-the-forgotten-bodybuilding-nutrient/
My understanding is that protein is important on a vA detox diet, otherwise the vA gets stuck in the liver. In this paper the man was protein deficient and vA toxic (I know this paper thanks to Naveen).
https://www.gastrojournal.org/article/0016-5085(82)90132-9/pdf
I’ve commented on that case study a couple times before.
What I think is remarkable is that this guy put on 26 pounds in 3 months in his 60’s, apparently just by changing his diet to include more protein, although he was also instructed to eat 3,000 calories per day, which sounds like quite a lot for a person of his age and stature.
What I speculate happened is that he put on fat stores after his dietary change. The increase in protein intake led to increased RBP production, which mobilized Vitamin A from the liver into the bloodstream, from which it got stored in newly created fat tissue around the body.
What is also remarkable is that at no point during the study did he show classic symptoms of Vitamin A toxicity outside of the liver. This seems to be in agreement with the idea that the Vitamin A in the liver went straight into fat stores where it was non-reactive for the time being.
Thus, the rate of Vitamin A “turnover” they calculated could just be a measure of how quickly the Vitamin A got deposited in fatty tissue.
A person on this forum claims to have healed themselves of eye problems likely related to Vitamin A and/or retinoid pharmaceutical use by adopting a low protein “fruitarian” diet. I have speculated that this happened by a path similar to the man in the case study, whereby lowered protein intake led to depleted RBP and therefore minimization of Vitamin A delivery to peripheral tissues, including the eyes.
This then led me to the question: is it better to keep excess Vitamin A stuck in the liver and risk liver damage (which might be more reparable than other tissue damage), or is it better to disperse it throughout the body, likely depositing it into whatever fat stores are available (could be the nervous system…not good!), and/or intentionally put on extra fat stores in order to store it safely until you can process it out of the liver at a higher rate.
Personally, I have low body fat and have always eaten a lot of meat, and I have experienced worsening symptoms after adopting a low Vitamin A diet. I suspect I sent a bunch of Vitamin A into my nervous system because there was no other place to put it. If the body knows best, then it appears it would rather risk damage to peripheral tissues and organs than keep Vitamin A bottled up in the liver.
Also, RBP has a short half life (Google says 12 hours), which makes me wonder...if you don't have fat to put Vitamin A into, and your liver is already overflowing with Vitamin A, then what happens when your protein intake fluctuates daily? Does that have much impact on your RBP levels, and if it does, is there a release of unbound Vitamin A somewhere in the body when the RBPs "expire" (not sure what actually happens to them).
That makes a lot of sense.
My biggest feature of vA toxicity was excessive, unexplained (very unfair!) weight gain that was very unusual for me. I think this was my body doing it’s best to sequester the excess vA out of the blood stream. I had other symptoms like pulse tinnitus and red gritty eyes but I think if my body hadn’t been a good fat maker I’d have been sicker.
After 3 years low vA I’ve lost just over half my poisoning weight. I’m assuming my body feels ready to give up the extra storage. It’s happened without a re emergence of my vA toxicity symptoms mentioned above.
Hi @yuri I’ve never done a log! I’ve commented over the past 3 years but never written out my experiences in one place.
I’m not doing anything particularly reportable. I just avoid the highest sources of vA and any in supplements/skin creams. I try to eat a nutritionally dense diet as I think the detox uses up nutrients, for processing and repair. I’m kind to my microbiome and liver. I try to live a low toxin lifestyle, sleep well, reduce stress, get out walking in nature and sun, drink plenty of water, use breathing techniques (search for ‘Dino’ for useful information on this) and I have monitored my minerals with Garrett Smith’s hair tests and supplemented accordingly. That’s been the plan. I’m not into rushing the process. Moderation is my middle name. I seem to be better now than I was so I’ll carry on in this way.
https://men-elite.com/2021/04/02/how-to-lose-fat-safely-while-peating/
"A few foods and substances that enhance this pathway (UGT enzymes) include cruciferous vegetables, citrus foods, dandelion, rooibos tea, honeybush tea, rosemary, ellagic acid, ferulic acid, curcumin, astaxanthin, ferulic acid, etc.
Foods that supply the D-glucaric acid for the UGT enzymes include: mung bean seeds, adzuki bean sprouts, oranges, spinach, apples, carrots, alfalfa sprouts, cabbage, Brussel sprouts, cauliflower, broccoli, grapefruit, grapes, peaches, plums, lemons, apricots, sweet cherries, corn, cucumber, lettuce, celery, green pepper, tomato, potato, etc.
After glucuronidation has added a glucaric acid, it’s ready for detoxification, but there is also an enzyme, beta-glucuronidase, that reverses the UGT conjugation reactions and preventing detoxification. Inflamed tissue contains high amounts of this enzyme so lowering inflammation would be key to keeping this enzyme low. Other things that lower the activity of this enzyme are saturated fat (polyunsaturated fat promotes this enzyme) and proanthocyanidins rich foods, such as strawberries, blackcurrant, cocoa, calcium, magnesium, vitamin C, Gotu Kola, etc. And last, but not least, my favorite for this, cardamom spice."
I wanted to provide an update here just in case someone were to stumble upon it. I tried Glucuronolactone for about a month and didn't notice much. Perhaps more energy a couple hours after ingesting, but it is hard to say for sure.