Anyone with longcovid checked ammonia levels?

Posted by longcovidcelsi @longcovidcelsi, Jul 4, 2023

Almost three years with longcovid here and no end in sight. 35, previously healthy, now totally debilitated. I can’t even fold a load of laundry without losing my breath and feeling nauseous.

Looks like for some people, shortness of breath could be caused by high lactic acid levels, but the source of THAT looks like a difficult-to-detect, acute liver injury from the virus that disrupts the urea cycle and leads to a back up of ammonia, which is itself a neurotoxin that creates an anaerobic environment which leads to the high lactic acid.
I’m getting my ammonia checked this week. Anyone else done this kind of lab?

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So what correction would medical treatment offer for ammonia levels?

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Hi! Lactulose, which is a sweet syrup laxative, is usually given to people with high ammonia levels. High ammonia levels do affect the brain.

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Profile picture for bettyjackson @bettyjackson

So what correction would medical treatment offer for ammonia levels?

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I’m not sure yet. Depends on what’s actually wrong with the liver, but it’s being suggested that reacting off the ammonia and lactic acid could help the liver calm down from its irritation and reset.

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I am finding improvement with an alkaline diet. I learned about this through a YouTube video posted in a different thread: “The Acid-Base Disruption Hypothesis for Long
Covid | With Vicky Van der Togt and Jeremy Rossman.”

It hypothesizes that with Long Covid our cellular metabolism can change from aerobic to anaerobic, which has a side affect of generating more acid.
Vicky Van der Togt posted on Twitter her results from using the Edge lactate meter (~$250 on Amazon): “ To say that the lactate levels we measured were shocking would be an understatement.
While normal lactate levels range from 4.5 to 19.8
milligrams per deciliter (mg/dL), or 0.25-1.1 mmol/l, we measured lactate levels at rest of over 100 mg/dl (or 5.55 mmol/l).”
She also shared her “makeshift treatment that I tried out on myself based on our hypothesis” (increases water consumption and a more alkaline diet).
Here is a link to their research paper: https://www.frontiersin.org/articles/10.3389/fimmu.2023.1150105/full

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My son who has long COVID had some tests done which showed elevated ammonia levels. Some research seems to indicate treatment with LOLA (L-ornithine-L-aspartate). Did you try this?

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So my understanding is that long COVID can reduce mitochondrial ATP production across the board.
The urea cycle, the process by which the body converts the waste product of protein breakdown, ammonia, into urea is highly ATP intensive.
Thus the urea cycle can be damaged without any long term damage to the liver (which is good news)
The bad news is this can lead to relatively mild ( relative to alcohol related liver disease) hepatic encephalopathy.
More good news, this is treatable.
More bad news, doctors are taught that urea cycle disorders are either genetic or as a result of a damaged liver.
Yet more good news, the support the urea cycle needs is available without prescription.
By eating the amino acids that your body expends enormous energy manufacturing, you save it that effort, the idea being that that energy can now be used deploying those amino acids in another ATP intensive activity, converting the ammonia into urea.
Then there are ammonia scavengers which will remove ammonia from your system using methods that don't involve ATP.
If you have the funds and a functional relationship with a physician who knows more about this than you do, the speak with them before ordering a bunch of amino acids and a food preservative.
And yes, the cells that make the amino acid substrates for the urea cycle, hepatocytes, are the same cells that convert the ammonia into urea, so, theoretically, the ATP saved in one intense process can now be deployed in an environment where there is enough substrate to convert the ammonia to urea.
So if you find eating more protein makes you worse, more tired, more irritable, less likely to make memories, or remember old ones (how many doctors understand that difference?), and/or NAD+ precursors make you worse, these are signs that you may, underscore may, have a urea cycle issue.
If you can eat double your usual protein and not worsen your situation it is highly unlikely that this is one of the issues affecting you.
If it is, manage your expectations.
This doesn't fix mitochondrial damage. It does mitigate the damage in one very specific, very necessary, process.
So it ain't a cure, no magic bullet, but possibly the foundation on which you can start to rebuild.
Good luck

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Profile picture for fqadpluslongcovid @fqadpluslongcovid

So my understanding is that long COVID can reduce mitochondrial ATP production across the board.
The urea cycle, the process by which the body converts the waste product of protein breakdown, ammonia, into urea is highly ATP intensive.
Thus the urea cycle can be damaged without any long term damage to the liver (which is good news)
The bad news is this can lead to relatively mild ( relative to alcohol related liver disease) hepatic encephalopathy.
More good news, this is treatable.
More bad news, doctors are taught that urea cycle disorders are either genetic or as a result of a damaged liver.
Yet more good news, the support the urea cycle needs is available without prescription.
By eating the amino acids that your body expends enormous energy manufacturing, you save it that effort, the idea being that that energy can now be used deploying those amino acids in another ATP intensive activity, converting the ammonia into urea.
Then there are ammonia scavengers which will remove ammonia from your system using methods that don't involve ATP.
If you have the funds and a functional relationship with a physician who knows more about this than you do, the speak with them before ordering a bunch of amino acids and a food preservative.
And yes, the cells that make the amino acid substrates for the urea cycle, hepatocytes, are the same cells that convert the ammonia into urea, so, theoretically, the ATP saved in one intense process can now be deployed in an environment where there is enough substrate to convert the ammonia to urea.
So if you find eating more protein makes you worse, more tired, more irritable, less likely to make memories, or remember old ones (how many doctors understand that difference?), and/or NAD+ precursors make you worse, these are signs that you may, underscore may, have a urea cycle issue.
If you can eat double your usual protein and not worsen your situation it is highly unlikely that this is one of the issues affecting you.
If it is, manage your expectations.
This doesn't fix mitochondrial damage. It does mitigate the damage in one very specific, very necessary, process.
So it ain't a cure, no magic bullet, but possibly the foundation on which you can start to rebuild.
Good luck

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@fqadpluslongcovid
I am a long covid victim, had fibromyalgia and a stroke before covid. All have same or almost systems.
What kind of foods help this issue ? How is this tested? Do we need to check liver damage first? Thank you I always question things now.

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Hi Leslon,
Thank you for your message.
So I could not agree more with your 'question everything' approach (personally, I don't identify as a victim because I find that narrative disempowering).
Let me start by saying the more I dig into this, the more complex it becomes.
Let's start with the testing
If low grade hyperammoniemia is the issue there is no reliable test. As soon as blood is drawn ammonia levels increase. The standard protocol is to keep the blood on ice and test it within 15 minutes of drawing it. The test results are not completely unhelpful in someone in end stage liver failure, but for detecting the small changes that can have a major, but non life threatening, impact, the test - to use the technical term - sucks.
As to liver damage, the damage is likely not irreversibly structural, but reversibly environmentally infrastructural.
As someone who has experienced ME and long Covid, you are probably highly aware of energy thresholds, and the practice of attempting to balance one's overall energy load.
From a dietary perspective, protein seems to be a key element. The more protein you eat the harder the liver has to work. Breaking down proteins creates ammonia, for a person who's liver has enough ATP, this is not a big deal, if you have ATP issues, it can be a very big deal.
So I would experiment with eating less protein and see if that helps, you can even try eating a high protein diet for a couple of days and see if that exacerbates your symptoms. That negative experience is the price you pay for learning if protein is an issue for you. If it isn't an issue, follow the general guidelines on protein intake. If it is, speak to your healthcare provider about how much you can safely reduce your long-term protein intake.
You may have to educate your healthcare provider about chronic acquires urea cycle defects as it is not currently taught in medical schools.
The good news is that, certainly for long COVID, and possibly for ME, the damage to the mitochondria is far more likely to be reversible compared to FQAD. What is required is an environment where it can recover, and part of that includes not having low-level ammonia toxicity which can lead to a vicious circle of symptoms which can feel unresolvable.
I hope this helps.
Good luck and best wishes,

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