uric acid

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NHE
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Re: uric acid

Post by NHE »

Hi Scott1,
Scott1 wrote: Mon May 23, 2022 5:12 am I don't take vitamin D and have never been sure about supplementing with it. Down here, even in our coldest months, we still have plenty of sunshine and I prefer to make it that way.
Have you ever had your vitamin D level tested? If so, what was the result? I’ve found that I have to take 5000 IU/day in order to maintain 45 ng/mL. Otherwise, it plummets into deficiency levels even with 1000 IU/day. Yes, I take 400 mg MgGlycinate per day so I don’t think it’s due to a Mg deficiency.
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Re: uric acid

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Whenever I've been tested its been around 48-50. I do go outside a lot and eat 2 boiled eggs everyday.
Different part of the world might make a difference.
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Re: uric acid

Post by Scott1 »

Hi,

I'm not so sure that the drug information you have sourced has said the right thing. Valacyclovir is an antiviral. If you read the notes attached to the B12 and K2 they are talking about antibacterials and antibiotics. That is definitely not related to how Valacyclovir works.
This note from the British Journal of Pharmacology gives a good rundown on it.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1615839/

Regards,
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Re: uric acid

Post by Anonymoose »

jimmylegs wrote: Tue May 24, 2022 3:16 am well i've clearly missed a few things here lol!

i just took a look at valtrex nutrient depletion (spoiler, B12 and K2):

Valacyclovir Drug Information
https://wa.kaiserpermanente.org/kbase/t ... hn-1534008

Calcium, vitamin D, vitamin K2, and magnesium supplementation and skeletal health (2020)
https://pubmed.ncbi.nlm.nih.gov/32972636/
"... Data suggest that VitK2 supplementation might improve bone quality and reduce fracture risk in osteoporotic patients, potentially enhancing the efficacy of Ca ± vitD. Mg deficiency could negatively influence bone and muscle health. However, data regarding the efficacy of vitK2 and Mg supplementation on bone are inconclusive."

The association of serum vitamin K2 levels with Parkinson's disease: from basic case-control study to big data mining analysis (2020)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485738/
"... Overall, the serum VK2 level of PD patients (3.49 ± 1.68 ng/ml) was significantly lower than that of healthy controls (5.77 ± 2.71 ng/ml)."

re vit D ouch, were you able to rule out magnesium and k2 as potentially low cofactors at the time?

ha thx, this topic has reminded me to put some nice gouda on the shopping list :D

not seeing much re potential valtrex interactions with the urea cycle so far.. kind of outside my limited wheelhouse!

Acute renal injury induced by valacyclovir hydrochloride: A case report (2016)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5228316/
Heya jimmy and all,

I’ve never tested mag deficient (or optimal) and I’m certain I was taking 400mg/day for some time before and whilst taking the d3-Valtrex. I seem to recall taking k2 a time or two and feeling a bit off w it so I stopped. I’ve never tested k2 level and I’ve got nothing against Gouda so maybe I’ll add it to my shopping list as well. :) B12 was too high after doing abx protocol so I doubt that was a problem at ouch times and there’s b12 in my multi and my iron supplement so prolly not an issue now either.

So far halving my coffee intake, backing off the citrus and other vitamin c rich fruits, and slipping a piece of nutchie toast in each day is working a charm. I suppose I should try hammering on b vitamins wo the NY to see if it’s the b’s or the purines fixing things up. However, now that I’ve stumbled upon the MS-UA association, I’m not abandoning the purine ship so that sloppy “science” ain’t happening.

From the gist of responses thus far, no one (of you THREE lol) is really into the uric acid thing anymore? What happened there? How could you not be into something that gives you an excuse to add bacon to your split pea soup?! I’ve got to do some more digging but not today.

Thx guys. Be well!
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Re: uric acid

Post by Scott1 »

Hi Anonymoose,

I am into a normal uric acid level. It is a goldilocks level: not too high, not too low.
People with MS generally have too low a level, so the question is why. This seems to have been ignored in recent years.
As I said earlier, uric acid is a breakdown product of ATP. To create ATP we need oxygen (watch that you are not iron deficient), CoQ10, Carnitine and B group vitamins. Magnesium and ATP bind readily together and are rarely separate for long.
Obviously, there is more to MS than just ensuring you have adequate levels of those inputs.
History has shown ideas about MS swing like a pendulum. e.g. The recent analysis on MS cases that had EBV infections in the US army is presented as new stuff but it was around in the 1990's, and then faded away, while the vitamin D arguments that were raging like a wildfire two years ago are more subdued today.
I still take 2x500mg of valacyclovir each day plus magnesium, CoQ10 and aceytl-l-carnitine. I no longer have any issues with fatigue. I do three (quite intense) pilates classes a week, get massaged and dry needled weekly to offset the effect of damage from past attacks. Given some of my motor pathways are affected, I also use Dantrolene Sodium to relax the tight muscles. Not many people use it because the neurologists prefer baclofen.
My mind has never been clearer and I get around without any aids whatsoever. From an original diagnosis in 1994 to now that's not too bad. The only time I got sick was in 2014 because I stopped taking the things I mentioned above and I ended up in a bad way. All my current problems stem from 2014, but they are less significant to me because I resumed doing the things that keep me well.

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Re: uric acid

Post by Anonymoose »

Scott1 wrote: Wed May 25, 2022 6:03 pm Hi Anonymoose,

I am into a normal uric acid level. It is a goldilocks level: not too high, not too low.
People with MS generally have too low a level, so the question is why. This seems to have been ignored in recent years.
As I said earlier, uric acid is a breakdown product of ATP. To create ATP we need oxygen (watch that you are not iron deficient), CoQ10, Carnitine and B group vitamins. Magnesium and ATP bind readily together and are rarely separate for long.
Obviously, there is more to MS than just ensuring you have adequate levels of those inputs.
History has shown ideas about MS swing like a pendulum. e.g. The recent analysis on MS cases that had EBV infections in the US army is presented as new stuff but it was around in the 1990's, and then faded away, while the vitamin D arguments that were raging like a wildfire two years ago are more subdued today.
I still take 2x500mg of valacyclovir each day plus magnesium, CoQ10 and aceytl-l-carnitine. I no longer have any issues with fatigue. I do three (quite intense) pilates classes a week, get massaged and dry needled weekly to offset the effect of damage from past attacks. Given some of my motor pathways are affected, I also use Dantrolene Sodium to relax the tight muscles. Not many people use it because the neurologists prefer baclofen.
My mind has never been clearer and I get around without any aids whatsoever. From an original diagnosis in 1994 to now that's not too bad. The only time I got sick was in 2014 because I stopped taking the things I mentioned above and I ended up in a bad way. All my current problems stem from 2014, but they are less significant to me because I resumed doing the things that keep me well.

Regards,
So glad you’re doing so well again. I’m a firm believer in adult neuroplasticity and use it or lose it mentality. Pilates is not my cup of tea though. Lol

It just occurred to me that *maybe* valacyclovir never gave you any issues because you’re male (flippin’ male privilege…grumble grumble) and you don’t take vitamin d so your UA levels didn’t drop low enough to cause the hurt/issues. Females typically have lower UA levels (and are more susceptible to ebv infection with low UA…so seems like UA optimizing goes along w the whole anti-ebv plan) than males and I’m sure that difference is even greater when the female is a lazy vegan.

I’ve a giant bottle of valacyclovir still…hmmm…I might have to test it out after a bit of serious purine loading. In its old, weakened state it’s got to be nicer to me now, right? But then if it works, I’ve got no source anymore. I guess I will have to brush up on my Buhner.

And YES, I know there is no evidence of V depleting UA but I’m still playing with that idea. If no one ever played with flimsy assumptions, we would never learn anything!

Off to crumble guilt free bacon on my breakfast taco. Life is good. :D

Be well
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Re: uric acid

Post by Scott1 »

Hi,
Watch the purine loading.
There is a difference between scratching and tearing it to ribbons!

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Re: uric acid

Post by Anonymoose »

Lol. No worries there. My purine intake is likely still in the low-moderate range. I like the bacon because I can just eat a little and get a good purine boost…going through a meat turns my stomach phase.

Creepy big brother has been watching and gave me a “Perlmutter on uric acid” video in my YouTube feed. Interesting. I’m thinking MSers have evolved to accommodate the change in our food supply so we’re like…more evolved. :roll: Msers get diabetes, don’t we? Have they identified why UA is low in MS? Is it genetic or part of the cascade?

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Re: uric acid

Post by Anonymoose »

Oo Oo Oo!!! Look at this…

https://www.ncbi.nlm.nih.gov/pmc/articl ... n_sectitle

Association Between Vitamin D and Uric Acid in Adults: A Systematic Review and Meta-Analysis

“According to our findings, high SUA might increase 25(OH)D level. This may be explained by the fact that hyperuricemia can inhibit 1α-hydroxylase and prevent the conversion of the 25(OH)D form of VIT D into calcitriol [1,25(OH) 2 D] 25 66 , hence increasing the level of 25(OH)D but decreasing the level of calcitriol. Genetic backgrounds may also be involved in these metabolic pathways as shown by evidence from genome-wide association studies 67 68 69 70 71 . For instance, the rs4588 and rs2282679 polymorphisms of GC (VIT D binding protein) gene and rs10766197 polymorphism of cytochrome P450 2R1 gene were highly associated with VIT D level 72 73 , whereas the rs2231142 polymorphism of adenosine triphosphate-binding cassette subfamily G member 2 (ABCG2) gene was associated with increased SUA level 71 . A Mendelian randomization study 74 also showed a causal association between the rs2231142 polymorphism of ABCG2 gene and VIT D through SUA by reducing urate transporter in renal proximal tubules. In the same site, the increasing SUA is associated with an inhibition of CYP27B1 gene expression for the 1α-hydroxylase enzyme, which converts 25(OH)D to calcitriol 66 . Furthermore, increased level of SUA might also lead to nephropathy in diabetic patients or initiation and progression of renal disease in non-diabetic patients, manifested as microalbuminuria due to hyperuricemia 75 , which might reduce the circulating VIT D binding protein and decrease VIT D level. Conversely, treatment with allopurinol, a xanthine oxidase inhibitor, in diabetic patients can decrease the SUA level and also increase the serum vitamin D level 76 . Therefore, the direction of the relationship between SUA and VIT D levels is still controversial.”

So it’s still all complicated and inconclusive but interesting to think about in context of low vit D and UA in MSers. Maybe coimbra works well in those w a high purine diet? Maybe that accidentally happens when they have to avoid calcium and vitamin c? What could 25(OH)D do for MSers w/o converting to calcitriol? Could the hypothetical accidental increase in uric acid really be responsible for coimbra benefits? What about keto…could that be a UA Trojan horse too (assuming coimbra is the first lol)? I wonder if there is a common MS genetic pattern in the mentioned metabolic pathways.

I grabbed some brewers yeast tablets today so no more fun w bacon.

Be well
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Re: uric acid

Post by Scott1 »

Hi,
"Have they identified why UA is low in MS?"

No is the short answer. I think its important to remember where UA lies in purine breakdown. It's the last step.There is a small school of thought that looks at purine signalling but the scientist who drove it (Geoffrey Burnstock) died of old age in 2020.
https://pubmed.ncbi.nlm.nih.gov/31646477/
A look at the science suggests it will be difficult for a drug company to focus on purine signalling as it would be unlikely to make money out of it.
Making ATP from scratch is a very slow process. Fortunately we can salvage ADP and rapidly turn it back to ATP (otherwise we are dead).
Increasing your uric acid as a goal means the focus is on the end stage of purine breakdown. I find it more helpful to focus on the first step where ATP is converted to ADP and back again.
Everything you do requires ATP. It is totally fundamental to being alive.
Rather than purine loading I concentrate on making sure I have the ready ability to make ATP.

You make ATP from ADP rather than store it. e.g. A 250g human heart has 0.7g of ATP in it at any one time. That is enough for 10 heartbeats so you need to make it readily on demand. You don't use it up and then replace it, you continuously replace it.
A similar thing happens in skeletal muscle. An elite athlete might run 100m in 10 secs but he can't turn around and immediately do it again as the ATP is used up. Same with weight lifters, they can lift a series of weights up to a limit then they can't go again because they have used up their easily available ATP. A lack of ATP makes muscles lock up. At the extreme you can see the effect when rigor mortis sets in.
To make ATP you need fatty acids, CoQ10, aceytl-l-carnitine, B group vitamins and oxygen. In your skeletal muscles the ADP is looking for a phosphate molecule. We store that in a phosphoryl group that needs oxygen to release it. Creatine helps provide the phosphoryl group. The easiest way to get that is from meat, otherwise you have to make creatine from a range of vegetable inputs.
So a diet that includes meat and dark green leafy vegetables plus the supplements mentioned above helps you make ATP.
Without denigrating Vitamin D, I'd ignore it and focus on making ATP.

Regards,
(p.s I do think that a disruption at the adenosine deanimase (an enzyme) level of purine breakdown is probably the cause of the low uric acid in MS. I would blame EBV for that but it's complex.)
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Re: uric acid

Post by Anonymoose »

Just popping on for a quickie :D

I doubt I have issues with ATP as energy is no issue for me. Yet I maybe ran into an issue with uric acid. And whilst, according to your recommendation to focus on ADP/ATP, you consume a diet rich in meat and greens, you are inadvertently focusing on purines methinks. Are you certain the ATP is the hero?

While going down the rabbit hole on my phone last night, I ran into some interesting stuff about purines and immune regulation. Maybe purines, not UA, are the missing elements for MSers. And valacyclovir and acyclovir are “purine-like.” Wonder what that’s all about. Does pyrimidine and/or it’s breakdown do anything to interrupt purine metabolism? I need to crack open my dusty laptop. This rabbit hole is too deep.

Be well
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Re: uric acid

Post by Scott1 »

Hi,
"Are you certain the ATP is the hero?"

I used to believe that energy wasn't an issue for me until I started to look at ATP. My assumption was, apart from the MS, I was normal. The difference in mental clarity and energy now is stark compared to what I thought was normal.

"you are inadvertently focusing on purines methinks."

I'm not inadvertently focussing on purines, I'm deliberately going to the top of the chain whereas focussing on uric acid is looking at the final breakdown product. To build ATP from scratch is very slow (about 100 days) so you need to preserve the ADP.

"Does pyrimidine and/or it’s breakdown do anything to interrupt purine metabolism? "

Nope.
Whether its a purine or a pyrimidine comes down to how many rings are in the structure. Purines have two and pyrimidines have one.

Acyclovir
There are three purine bases which when attached to a ribose become nucleosides- adenine/adenosine, guanine/guanosine, and hypoxanthine/ inosine. The acyclovir is almost the same as the guanosine except it lacks a hydroxyl group at the third carbon. When it slots into an viral RNA ribbon instead of guanosine triphosphate there is nothing for the next group to attach to so the chain of viral RNA terminates at that point. That is how acyclovir works. It stops replication, it doesn't destroy the existing virus but over time your viral load declines through natural attrition of the host cells (EBV resides in B cells).

How does vitamin D fit into this?
The components of ATP come from the foods we eat (amino acids from protein, glucose from simple sugars, and fatty acids plus glycerol from fats). In a well functioning system, they eventually convert into aceytl-CoA and continue to be broken down. Ultimately, we divide them into molecules of carbon and oxygen (i.e. CO2) and hydrogen. That lets us exhale CO2 and use the hydrogen in the electron transport chain (inside the mitochondria) to make ATP.
There's obviously lots of other pathways at work at the same time. One of those sees some aceytl-CoA follow a different pathway (with about 130 steps) that turns into lanosterol. That is the precursor for cholesterol and 7-dehydrocholesterol. The latter is also known as provitamin D which sits in our tissues near the skin. It has 5 rings that are closed. When we are exposed to sunlight, one of those rings opens (called the B ring) and the structure's name changes to previtamin D. In this form it migrates from the tissue to the blood stream. Eventually we turn that into cholecalciferol then into calcidiol and then calcitriol. That is the form that is functional for gene transcription. The problem is all these forms love fat so if you tend to carry too much body fat it will act as a sink and hold the vitamin rather than use it.
For these pathways, the worst thing you can do is take a statin. To block cholesterol formation it disables an enzyme called Hydroxy-3-methylgluataryl-CoA reductase (a mouthful, I know). It certainly stops cholesterol but it also stops CoQ10 formation, consequently affecting formation of ATP and vitamin D formation.

Regards,
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Re: uric acid

Post by Anonymoose »

Hey scott1,

Thanks for your answers. I did a bit more googling whilst chasing various other squirrels and ran into (and unfortunately later closed the related window) a study that explained lower uric acid levels noted in another inflammatory condition are the result of “consumption” of the uric acid as an anti-oxidant to neutralize by-products of inflammation. Back to the boring old inflammatory cascade. Sigh. I guess UA is still good to have around so I’ll stay on top of it anyway. ….And I guess that allows a lot of room for Valtrex to be involved in the ouch too so there’s that.

Back to your regularly scheduled program :)

Be well
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Re: uric acid

Post by jimmylegs »

this adult onset vegan case report interested me:

Adult-onset presentation of a urea cycle disorder necessitating intensive care unit admission
https://link.springer.com/article/10.10 ... 20-01618-3

from that, i can't tell if they bothered to look at zinc status.

i was eating high purine meats trying to restore ua status for a while, but it only stayed flat or even got lower. i never did measure my ammonia levels, but comparing to other studies, if mine was at all similar my levels must have been atrocious and i expect were responsible for some pretty profound cognitive impairments at the time.

only once i finished a really high dose zinc regimen, over at least a month, did ua start to behave and went up to 278. i've maintained my zinc levels ever since, with attention to copper and ferritin status to be on the safe side, and have considered the ua problem solved. :)
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Re: uric acid

Post by jimmylegs »

i looked back over things here and yes scott, re your post of may 25 i trusted the kaiserpermanente site (mea culpa!), when meds are really not my wheelhouse at all :o
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