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Foamy Urine
This is a very interesting thread, thanks guys! I've definitely seen foamy urine come and go. I want to say that it seems to me a "first thing in the morning" type of thing. @ourania sometimes talks about the body's daily schedule... there could be a clue in there.
Thanks Jenny. For my own case, I have lower liver enzymes and GGT, so cholestasis is not obviously what is going with me. So maybe for me the foamy urine is not from bile salts. Who knows?
Yes who knows? We are all on a path of discovery here. I’m interested in the biology of toxicity/detoxification and what can go wrong, but how each of us fits into this is going to be personal.
I think some people will have got vA toxicity by massively overdoing vA whereas others may have got toxic from more moderate amounts of vA because their detoxification pathways were already compromised, vA toxicity then makes everything worse. I suspect most people will have some sort of combination. Recovery from vA toxicity is going to be influenced by what put you there.
I’m personally in the latter category I think. I’m building up a nice picture of everything I inadvertently did wrong!
I've been experiencing foamy urine, constantly when I first began low a, then tapering off, and now ramping up again here at a little over 6 months. This is foam that sticks around for over a minute, so quite noticeable.
Mainstream medicine will tell you flat out that this is a telltale sign of CKD...
I found a post by Grant, Protein Synthesis and Setbacks, February 5, 2019:
I think what’s happening is that as the regular vitamin A serum levels start to decline, then just due to the mechanism of chemical equilibrium, more stored vitamin A is released from the liver. That’s just what we want to have happen right? Unfortunately, there’s a catch to it. There is a relative toxicity scale to the various forms of vitamin A. Obviously, retinol captured in the RBPs is not very toxic at all, next up is unwrapped retinol, and then it’s the retinyl esters, followed by retinoic acid. So, that storage form in the liver is actually quite toxic. And with it now being released faster than usual, people would experience its increased toxicity.
The following is from a 1981 report by Anthony R. Mawson and Gabriel I. Onor titled: Gout and Vitamin A Intoxication: Is There a Connection?
Retinyl esters react more randomly with the membranes of cells than the physiologically sequestered retinol bound in holo-RBP; hence, they are a major form of vitamin A toxicity.
Other sources back up and confirm this information.
Additionally, much of the liver’s retinyl esters are in the retinyl palmitate form, and that’s a more water-soluble molecule. Thus, that might explain why some people are experiencing foamy urine after being on a low vitamin A diet for a while.
This is to reassure anyone else here who is experiencing this condition. I know Hermes was stumped by it back in 2023 (I just did a forum search for foamy urine).
I see also that foamy urine can be about phosphorus in CKD. It's a bit confusing and I'm not really sure how it all works. But kidney patients usually cut back on phosphorus.
Now I know I get the two Josephs here mixed up, but are you the one who has recently sworn off the heavy beer intake? Could this possibly be about phosphate, thiamine and refeeding? (ie, your sudden lift in thiamine is drawing down your phosphate too quickly?)
https://ggenereux.blog/discussion/topic/hypophosphatemia-and-thiamine/
Proper phosphorus balance seems related also to calcium and therefore vD too, and milk seems to be one option, as the poster Romaine mentions.
I have had slightly foamy urine right along, not that that is good LOL, I just don't try to micro-manage myself. If the urine wants to be a bit foamy, I just accept it, LOL. As you can see in the rest of my post here, Phosphorus levels are pretty complicated. I just wanted to point out that you might be going through a phase.
@lilchick
I learned a bit about thiamine and phosphorous from your lead. It seems I'm getting plenty of thiamine (in fact more than ever before in my life) from my staples of brown rice, black beans and beef.
From the thread you linked:
Refeeding syndrome is something they watch out for when treating anorexic patients. The explanations I read said that it is caused when your body switches from catabolic (breaking down tissues) to anobolic (rebuilding tissues) metabolism which puts a great demand on certain nutrients. It is also a risk in alcoholic patients which is interesting as when being treated and withdrawing from alcohol alcoholics need extra thiamine (for the alcohol dehydrogenase system I believe).
I think you're right that my body is switching to rebuilding and needs more resources to accomplish this. Low calcium is possible but I eat half a cup of boiled oats with maple syrup every morning and always my beans so I doubt it. I found this:
Episodes of acute infection are thought to deplete body stores of vitamin A. The mechanism by which this might occur is not known, but increased metabolic requirements are presumed to play a role. We have found, however, that significant amounts of retinol and retinol-binding protein (RBP) were excreted in the urine during serious infections, whereas only trace amounts were found in the urine of healthy control subjects.
https://www.sciencedirect.com/science/article/abs/pii/S0002916523184425
I don't have an infection but I think the mechanism is the same: the body is taking an opportunity to throw ballast overboard. Whether that opportunity is due to an acute infection or a deplete diet the result is the same. There are definitely echoes of Grant's "Yamoto syndrome" here.
I believe that it's better to get this vile poison out steadily and bit by bit as opposed to all at once. All at once is that cascading scenario Grant mentioned in his first book, and it often results in cancer. I can't find Grant's citation, but after some digging I found an excellent article which mentions this "retinoid cascade" in regards to covid:
Building on these observations, we propose that infection-induced activation of the retinoid cascade triggers cell-mediated apoptotic hepatitis, leading to transient cholestatic liver dysfunction, in which stored vitamin A compounds (retinyl esters and the metabolite retinoic acid) enter the circulation through damaged bile ducts and hepatocytes; this exposure can in turn cause lung injury and other organ damage by apoptosis, necrosis, and acute neutrophilic infiltration (21). On this hypothesis, an endogenous form of retinoid toxicity contributes to the multiple signs and symptoms of COVID-19, and disease severity is directly proportional to the concentration of circulating retinyl esters and retinoic acid.
It's always good to remind ourselves why we do what we do 🙂