ME/CFS, Fibromyalgia, and Long COVID – the “Metabolic Derangement” Diseases?

[SWAlexander]

I´m very glad that Cort Johnson published this very good article.
At the same time it is very frustrating that doctors in Germany refuse (for whatever reason) to test VLCFA even though I delivered previous results (tested in USA 2018) for elevated phytanic acid.

I mentioned " New article on VLCFA / ALD or X-linked (high phytanic acid)" back in
Mar 17, 2022 https://forums.phoenixrising.me/thr...cephalomyelitis-icc.85648/page-7#post-2387779

Now comes the challenge (again) to find a doctor who is willing to take my blood even though I would pay for the test. The excuse is always the same, "we don't know how to tread "Metabolic Derangement" (fatty acid phytanic acid). This is BS.
BTW most US insurance will pay for in full.

I would like to encourage everybody to read the article.

https://www.healthrising.org/blog/2...-syndrome-fibromyalgia-metabolic-derangement/

Excerpt:

• A University of Colorado/Jewish Health Center team jumped on long COVID early and in mid-2020 began having their patients do exercise tests.
• That resulted in an earlier paper that found significantly lower levels of fatty acid oxidation in all 50 of the long-COVID participants. Because fatty acids provide an energy source for our mitochondria, problems with fatty acid oxidation or breakdown could help explain the fatigue and exercise problems in long COVID.
• Their goal in their latest study was to see if their metabolomic findings matched up with their earlier findings; i.e., did they indicate, on a molecular level, that problems with fatty acid metabolism and lactate production were present?
• The study did – to the extent that the authors referred to the “metabolic derangements” found. The study found evidence that fatty acid metabolism was impaired and the long-COVID patients were turning to less efficient amino acids to power their mitochondria.
• They also found evidence of problems with taurine and tryptophan metabolism.
• The authors stated that “compelling evidence of metabolic dysfunction in PASC (long COVID)… that should fuel future investigations of oxygen and lactate kinetics and mitochondria biology. Interventions aimed at restoring promoting mitochondrial activity and restoring fatty acid oxidation should be explored.“
• Then, ignoring the dozen or so ME/CFS studies that have found similar metabolic issues, they turned to sepsis and type II diabetes to explain how their findings could help explain exercise intolerance.
• Interestingly, similar findings in fibromyalgia (FM) have recently shown up.
• ME/CFS with its bigger, more complex metabolomic studies is ahead of the game and several causes (peroxisomal dysfunction, hypoxia, mitochondrial problems) have been proposed.
• With the exception of some ME/CFS studies, most of the studies have been small and these findings need to be validated. Still, they suggest that core metabolic abnormalities may be present in long COVID, ME/CFS, and FM.

 

[Wishful]

The issue I have with this hypothesis is that with all the mitochondrial-modifying treatments people have tried, there doesn't seem to be much evidence of them affecting the symptoms. Sure, a few people report that "supplement x reduces my ME symptoms", but this is ME, where we don't understand what's going on in our bodies, and it varies with the individual. Just because supplement x has one theoretical mechanism for affecting mitochondrial function doesn't mean that it's the mechanism that provides the observed benefit.

Also, since my ME doesn't involve reduced physical capacity, my guess is that my blood and muscles would show no sign of impaired fatty acid metabolism. It's possible that my brain metabolism is impaired without affecting cells in the rest of my body, but I think it's more likely that these observed metabolic dysfunctions are a downstream effect of ME and PASC.

 

[SWAlexander]

The issue I have with this hypothesis is that with all the mitochondrial-modifying treatments people have tried, there doesn't seem to be much evidence of them affecting the symptoms.

This makes sense.

Just because supplement x has one theoretical mechanism for affecting mitochondrial function doesn't mean that it's the mechanism that provides the observed benefit.

Maybe not supplements bring lighter symptoms.
It made a big energy difference to me since avoid meat and by-products from animals with ruminant stomachs cattle, sheep, goats and dark green vegetables. It had eased symptoms such as severe headaches and muscle weakness besides the most irritating presents of smells like methane gas.
I had the VLCFA test that showed elevated Phytanic acid.

 

[Husband of]

Also, since my ME doesn't involve reduced physical capacity,

Sorry, What do you mean by this?

 

[Wishful]

Sorry, What do you mean by this?

Many (most?) PWME suffer from reduced physical capacity: they can't do the same level of exertion as before developing ME. Some also have reduced strength. I never had those reductions. I could still hike, bike, saw/split wood, dig soil, etc, for hours. Some activities might trigger PEM (after only minutes of those activities), while others wouldn't even after hours of those activities. So from my experience with my ME, symptoms of reduced capacity are downstream effects and not an essential part of ME.

 

[Wishful]

It made a big energy difference to me since avoid meat and by-products from animals with ruminant stomachs

I'm not surprised that you found something that made your ME worse. There are all too many food components that I have to avoid. What I was saying is that we don't understand the mechanism for these abnormal responses. Some people believe in a hypothesis, such as ME being due to mitochondrial dysfunction. If they encounter an observation that supports that hypothesis, such as a food that supposedly (not scientifically proven) boosts mitochondrial function, they accept it as absolute proof of the hypothesis. However, there are probably a vast number of alternative mechanisms for how that food could cause the observed effect. They would need to try other foods/nutrients that work via the same mechanism and see whether they produce similar results.

 

[tyson oberle]

This makes sense.


Maybe not supplements bring lighter symptoms.
It made a big energy difference to me since avoid meat and by-products from animals with ruminant stomachs cattle, sheep, goats and dark green vegetables. It had eased symptoms such as severe headaches and muscle weakness besides the most irritating presents of smells like methane gas.
I had the VLCFA test that showed elevated Phytanic acid.

View attachment 50072

So what is the solution for high phytanic acid? Is it to only "avoid meat and byproducts from animals with ruminant stomachs and dark green vegetables"? So are you saying you only avoid meat from animals with ruminant stomachs? And if yes, so I can understand, what is the difference between ruminant meat and non-ruminant meat in causing issues? And do you also avoid dark green vegetables? And if yes, what is in dark green vegetables that cause issues? Do you also take carnitine, creatine, CoQ10, folic acid, alpha-lipoic acid, MCT oil or anything else that was recommended? Did you reduce long chain fatty acids in your diet?
I want to do this VCLFA test. Is it hard to get a doctor in the USA to order this?

 

[Husband of]

Many (most?) PWME suffer from reduced physical capacity: they can't do the same level of exertion as before developing ME. Some also have reduced strength. I never had those reductions. I could still hike, bike, saw/split wood, dig soil, etc, for hours. Some activities might trigger PEM (after only minutes of those activities), while others wouldn't even after hours of those activities. So from my experience with my ME, symptoms of reduced capacity are downstream effects and not an essential part of ME.

Thanks, that's interesting, the first I've heard that people with ME may not have reduced physical capacity. I assumed you must have meant something else.

FWIW, while I had (actually still recovering) COVID, and more so at the start, upon minimal physical or mental exertion I would feel sick, increased heart rate, dizzy/spaced out feeling, brain fog, nausea, seemingly in a similar way to what my wife does.bi don't know if there are any clues in that.

do you get POTS?

 

[Rufous McKinney]

Maybe not supplements bring lighter symptoms.
It made a big energy difference to me since avoid meat and by-products from animals with ruminant stomachs cattle, sheep, goats and dark green vegetables. It had eased symptoms such as severe headaches and muscle weakness besides the most irritating presents of smells like methane gas.

I agree foods can have major effects on the body...chinese traditional medicine is very focused on the diet. (no wonder westerners just want a Pharma pill)

I specifically avoid dark green leafy vegetables (termed "bitter") also because they are contraindicated when you experience "wind" and digestive challenges.

What was the cow, the sheep the goat fed?

1) glyphosate (commercial grains are laced with this substance) (known to cause non-hodgkins lymphoma)

2) not grass fed: ruminants eat grass, not Soy Beans

3)GMO- something we don't know alot about but makes some of us nervous depending.

My digestion was disrupted by something last night. What? Ate green leafy at dinner, something I normally avoid. Maybe its just mild PEM from overdone yesterday.

 

[Rufous McKinney]

And if yes, what is in dark green vegetables that cause issues?

in chinese medicine, bitter greens can cause wind. so if your out of balance, more wind = loose stools, bloat etc.

The basic diet I do well on with an IBS-d type system is warm oily smooth. (bitter greens are not smooth)

 

[SWAlexander]

Is it hard to get a doctor in the USA to order this?

Yes and no. Like I said before many doctors never heard of VLCFA and don't know what lab would test, nor do they know the Lab code. But a call to ARUP Laboratories or visiting the website has answers about test requirements.

This PDF by ARUP Laboratories provides details.
This test will provide information about X-Linked Adrenoleukodystrophy Testing a genetic mutation in the ABCD1.
It can provide information if it is X-Linked or Refsum Disease (https://rarediseases.org/rare-diseases/refsum-disease/).

 

[lyran]

It is strange they found low tryptophan levels in the study. In some earlier studies tryptophan levels have been high and tyrosine levels low.

 

[SWAlexander]

tyrosine levels low

I know. For this reason, I tried tyrosine. The results were these reactions; nausea, bad headache, heartburn and restlessness.

 

[lyran]

I know. For this reason, I tried tyrosine. The results were these reactions; nausea, bad headache, heartburn and restlessness.

Tyrosine raises dopamine and norepinephrine. Maybe one or the other is already high?

When I take tyrosine, I get a calm feeling and a slight dopamine boost later in the day. It does cause insomnia if I take it too late in the day.

 

[Wishful]

Thanks, that's interesting, the first I've heard that people with ME may not have reduced physical capacity.

We seem to be a small subset. Some other people here reported that they had ME, but were still able to continue bodybuilding activities that I found quite impressive (and way beyond me). There seem to be enough of us that I am convinced that ME is not a metabolic or mitochondrial disease; physical limitations are just a (unfortunately common) downstream effect.

 

[SWAlexander]

Tyrosine raises dopamine and norepinephrine. Maybe one or the other is already high?

Thanks. I wish I could have these 3 catecholamines tested: epinephrine (adrenalin), norepinephrine, and dopamine. They don´t do it in Germany.

 

[SWAlexander]

physical limitations are just a (unfortunately common) downstream effect.

I believe so too. The question remains "downstream effect" caused by what?
Is it as one UK doctor told me PPS?
I´m searching for this answer forcefully since 2014.
There is no single test for PPS and research has not been great about it.

 

[Violeta]

What causes reduced fatty acid oxidation?

This study says that:

Beta-oxidation is a significant source of metabolic energy during interprandial periods and high energy demand states, such as exercise. These metabolic conditions induce the release of fatty acids from adipose tissue due to the secretion of circulating mediators, such as epinephrine and glucagon, which increase the rate of lipolysis. This metabolic pathway provides a large portion of the energy requirement of skeletal muscle, heart muscle, and kidneys when glycogen and gluconeogenic precursors become scarce.

https://www.ncbi.nlm.nih.gov/books/NBK556002/

 

[Violeta]

Another factor related to fatty acid oxidation is availability of oxygen.

Also from the study:

Other factors that regulate beta-oxidation include adequate oxygen supply for the continued electron acceptance from carrier substrates produced, namely FAD(H2) and NADH, to maintain a pool of electron acceptors available. Expression of enzymes involved in fatty acid oxidation becomes upregulated through fatty acids behaving as ligands that bind to peroxisome proliferator-activated receptors (PPARs); these transcription factors form homo-/heterodimers and translocate to the nucleus, where they alter gene expression involved in the production of proteins required for beta-oxidation and mitochondrial biogenesis.

https://www.ncbi.nlm.nih.gov/books/NBK556002/

 

[Husband of]

t is strange they found low tryptophan levels in the study. In some earlier studies tryptophan levels have been high and tyrosine levels low.

there was a Japanese article that came out at basically the same time as the Ron Davis one in 2015 with some opposite results. I wonder if it has to do with different populations having different metabolic processes, based on genes.

I'm no expert but I do find it odd how often scientists look at bodily processes in one population, or even sometimes a single person, and assume the same process applies to all people.

I am convinced that ME is not a metabolic or mitochondrial disease

the Itaconate shunt theory also assumes the metabolic issues, caused by the shunt, are downstream. They've been promising a video to explain what might be causing the shunt for a while now.

Under the Itaconate shunt hypothesis they hypothesize that different severity levels for pwme could be explained by the number of cells in which the shunt is occurring. You could extend that to say different synptomology could be explained by which cells are affected.