Could and upset liver be a clue to Me/cfs?

[Rufous McKinney]

Dr. Prusty has something about liver problems

https://twitter.com/i/web/status/1606571371366158336

"1. In an attempt to find a biomarker(s) that differentiate severe patients from mild/moderate patients, we came across some genes which are significantly altered in severe patients. We are not accessing correlation with viral infection at this moment.

2. As these genes have something to do with liver and lower respiratory tract, I am trying to see their relevance to the severity of the disease. Sometimes genes can also have a completely different function than the known ones."


Now I am very curious about lower respiratory tract....

 

[Rufous McKinney]

ower respiratory tract....

oh. thats is basically everything windpipe and below: its our lungs.

 

[wastwater]

Lowering of complement C3 maybe resulting in an immunodeficiency that’s under reactive to bacteria especially in the younger years and over reactive to viruses
Also FOXO is in the liver

 

[Consul]

Impaired gluconeogenesis, read full thread

https://twitter.com/i/web/status/1665842992979091457

Also Karl Morten says they are doing a big metabolomics study

 

[Judee]

Impaired gluconeogenesis, read full thread

https://twitter.com/i/web/status/1665842992979091457

Also Karl Morten says they are doing a big metabolomics study

Wow...that is so interesting esp what she said during sleep and exercise...I wonder if that might explain why the first part of our day is also so lousy for so many of us too.

I was asking in a group on FB recently about a low LDH result.

From that twitter post Consul posted: "ME/CFS patients also have higher than normal lactate after exercise, as gluconeogenesis is supposed to take up lactate and turn it into glucose during exercise, this could suggest this process is impaired in ME/CFS patients."

Does anyone understand how LDH relates to gluconeogenesis and if low LDH could impair that?

I've never had that test before...it was a part of a package of tests I purchased but makes me wonder if anyone else here has been tested for that and if their results were similar. ??

 

[SlamDancin]

Just want to shout out my friend @mariovitali who I saw on S4me was one of the reviewers of this paper. Great to see that

 

[Consul]

New theory of long covid, possibly because of liver problems.

https://www.mdpi.com/2075-1729/13/7/1462

 

[CSMLSM]

I had elevated bile acids

I myself recently this year self diagnosed myself with cholestasis, implemented a treatment regime for it and corrected/understood many things that had an unknown cause. It has answered many questions for me and greatly improved my health.

Below is information on intrahepatic cholestasis in pregnancy but is still relevant to us non pregnant people.

As you can see elevated bile acids is one indicator and also raised bilirubin.

The bile acids and bilirubin is higher as it cannot leave the liver as it should so makes its way into the blood stream and this is also the case with cholesterol I believe.

Bile in part is made from cholesterol

https://www.smfm.org/publications/96-understanding-intrahepatic-cholestasis-of-pregnancy#:~:text=Diagnosis/definition: Intrahepatic cholestasis should be suspected when pruritis,of patients will have increased direct bilirubin levels. Diagnosis/definition: Intrahepatic cholestasis should be suspected when pruritis develops in the absence of a rash. Lab evidence of cholestasis includes elevated bile acids (> 10 umol/L). Up to 60% of patients will have elevated transaminases and 20% of patients will have increased direct bilirubin levels.

https://www.verywellhealth.com/cholestasis-overview-4586590 Cholestasis is a reduction (or cessation) in the flow of bile. Cholestasis can occur at any age in both males and females. This can happen for several different reasons. Cholestasis can occur from impairment of bile secretion from the liver cells, an obstruction that blocks the flow of bile, or a combination of the two.


Bile is a greenish-brown fluid that aids in digestion and is secreted by the liver and stored in the gallbladder. The lack of any of the substances that are normally secreted into bile can cause cholestasis. These substances include:

• Water
• Cholesterol
• Lecithin (a phospholipid)
• Bile pigments (bilirubin and biliverdin)
• Bile salts and bile acids (sodium glycocholate and sodium taurocholate)
• Copper and other excreted metals (in small amounts)

Maybe you also have had low vitamin D test results and low vitamin B12 as bile is needed for the absorption of fat soluble nutrients and is also required for the enterohepatic circulation recycling of vitamin B12.

I was thin and sporty

Bile is also needed for the absorption of fat, acting as an emulsifying agent allowing the absorption of fat and the calories it contains.

Also if you do not consume/absorb cholesterol then the liver will make more as it is vital for health believe it or not.

Bile is also needed to absorb Omega 3, a fat.

So low D, low B12 and low Omega 3 are all common in ME/CFS.

Also Epstein–Barr virus (EBV) is commonly thought by many to be a key factor in ME/CFS and this virus causes liver damage when caught. Given we are likely susceptible to EBV this damage or influence may linger.

https://pubmed.ncbi.nlm.nih.gov/21238898/ Objectives: Epstein-Barr Virus (EBV) infection has the potential to establish life-long, benign infections in their hosts. Although biochemical evidence of hepatocellular damage is common, jaundice is uncommon and complete recovery is the rule. The present study describes clinical characteristics and changes of liver function tests during the course of infectious mononucleosis. Conclusion: Liver involvement in acute EBV infection represents mild and self-limited hepatitis with predominantly cholestatic features.

I am currently in full remission of ME/CFS due to a treatment regime I have spent many years on.

Discovering I had issues with cholestasis was the last part of the puzzle.

 

[mariovitali]

@CSMLSM Would you like to describe your regimen? I am also in full remission as long as I follow a specific regimen related to improving liver function

 

[CSMLSM]

@CSMLSM Would you like to describe your regimen? I am also in full remission as long as I follow a specific regimen related to improving liver function

Hi @mariovitali,
So as I have bile flow issues due to cholestasis I take TUDCA on an empty stomach early in the day. TUDCA is a bile acid/salt and gets absorbed and contributes to increasing bile and thus flow.

Because I have had this cholestasis for so long undiagnosed I believe it has affected my pancreases ability to produce digestive enzymes and my ability to fully digest food has been affected. For this I take an ox bile supplement and digestive enzymes with a meal.

I also take apple cider vinegar before the meal to help acid levels and to help activate some of the digestive enzymes.

Due to being unable to absorb fat, fat soluble nutrition and recycle B12 properly for so long I take omega 3 supplements, vitamin D (less now during summer) and take intramuscular methylcobalamin form of vitamin B12.

I also take other supplements which are-
Methylated B vitamin complex
Vitamin K2 MK-7
Iodine
Zinc with copper
Potassium citrate
Epsom salt baths for magnesium as I feel that this is a quick way to increase magnesium levels without side effects and is superior to oral supplementation.

The magnesium and potassium are important for the electrolyte loss we tend to suffer from as ME/CFS patients.
Potassium is only able to be held onto in the body when you have good magnesium levels so at first I only took the epsom salt baths and then added the potassium later. I was having 2-3 epsom salt baths a week and now about 1 a week.

I believe the theory of Epstein–Barr virus(EBV) infection plays a major role in ME/CFS and I take a molecule that targets the cells that are infected and makes them apoptose(programmed cell death). This molecule is caryophyllene and it targets CB2 receptors on B cell immune cells that are infected with EBV, other immune cells and helps the immune system to get closer to homeostasis(balance) and is a selective agonist of the CB2 receptor.

It also acts as an enzyme inhibitor of fatty acid amide hydrolase(FAAH). This enzyme is responsible for degrading a molecule called Anandamide which binds to CB1 and CB2 receptors as an agonist.

I also take cannabidiol(CBD) which supports this activity. CBD also acts as an enzyme inhibitor of FAAH but does not bind to CB1 and CB2 receptors as an agonist but antagonist/inverse agonist type action which improves receptor and agonist action tone. This prevents tolerance and basicly improves the way it all works together.

I buy CBD isolate and vape this using a 80VG/20PG base mix to add it to at about 1.5g CBD isolate per 30ml base liquid.

To source the caryophyllene I use a natural product called Copaiba essential oil which I only use the steam distilled kind for safety.

I will be looking into an isolate of caryophyllene but for now the source I have obtained is plenty and pleasant to vape as well.

I mix this at a rate of 1ml copaiba(approximate 40% concentration of caryophyllene according to the supplier which is exceptional) to 4ml base liquid.

 

[mariovitali]

@CSMLSM Thank you for your reply and I am so glad you are well. Please have a look at the following thread which I posted in 2015.

https://forums.phoenixrising.me/thr...ponse-and-a-possible-treatment-for-cfs.37244/

TUDCA was also a game changer for me as it reduces endoplasmic reticulum Stress and of course it is one of the best liver protectants. Our regimens are quite related. I also take methyl donors , Vitamin K2, Omega3, TUDCA and have complete abstinence from alcohol.

Thank you again for your post !

 

[CSMLSM]

@CSMLSM Thank you for your reply and I am so glad you are well. Please have a look at the following thread which I posted in 2015.

https://forums.phoenixrising.me/thr...ponse-and-a-possible-treatment-for-cfs.37244/

TUDCA was also a game changer for me as it reduces endoplasmic reticulum Stress and of course it is one of the best liver protectants. Our regimens are quite related. I also take methyl donors , Vitamin K2, Omega3, TUDCA and have complete abstinence from alcohol.

Thank you again for your post !

I am glad you are doing well too

I will take a look when I have the time as I want to give it a decent look over, I am doing like approximately 12h days of activity now but had a few days of rest recently drinking some elderflower and cranberry wine I made myself, its 15% alcohol and was super strong.
I am fine now and have no after affects.

I recently heard back from specialist my liver function tests are all normal now following my treatment with TUDCA, ox bile, digestive enzymes, cannabidiol and caryophyllene(from copaiba essential oil). They have always shown something off like raise ALT and bilirubin but now all normal.

I was waiting for a faecal elastase test result but it was likely lost or something went wrong and I have to retake the test.
It will show if my pancreas is under producing digestive enzymes.

Thank you for your interest!

 

[Violeta]

I am wondering if or how liver issues affect whole body oxidative stress levels.

I found this about non-alchoholic fatty liver. It causes oxidative stress in hepatocytes, but do you think it causes oxidative stress elsewhere in the body? For example, in the eyes?

"The mechanism of ROS-mediated oxidative stress and lipid metabolism in hepatocytes. In the NAFLD patients, the overload intake of free fatty acids increases fatty acid β-oxidation and electron transport chain activity in the mitochondria. This ultimately leads to an increased release of ROS as byproduct of metabolism."

Besides NAFLD, is there any other way to approach looking into this?

Edit in: viral infections

And PS: just saw that liver issues cause itchy skin.

 

[Violeta]

Role of Oxidative Stress in Pathophysiology of Nonalcoholic Fatty Liver Disease​

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6016172/

In this paper, we will review the main evidences on the strict pathophysiologic linkage between oxidative stress mechanisms and the presence NAFLD and its progression, particularly focusing on the most reported pathophysiological mechanisms: mitochondrial dysfunction, endoplasmic reticulum (ER) stress, iron metabolism derangements, gut-liver axis, insulin resistance, and endothelial dysfunction.

I guess this paper will cover the question.

 

[mariovitali]

@CSMLSM Just FYI, after using Ox bile for 6 months , I ended up having a cyst in my gallbladder which I now have to monitor.

 

[CSMLSM]

@mariovitali thank you for sharing this. Do you happen to know how it may have caused this? Maybe I should increase TUDCA and just take digestive enzymes.

 

[mariovitali]

@mariovitali thank you for sharing this. Do you happen to know how it may have caused this? Maybe I should increase TUDCA and just take digestive enzymes.

The only thing I could think of , is that those who have not removed their gallbladders (I have mine) , we do not need additional bile acids but instead we want to fix the composition of them ( and I believe TUDCA does that). Remember there exists lots of bile acids types.

 

[CSMLSM]

Remember there exists lots of bile acids types.

we want to fix the composition of them

Good points, when I started the TUDCA, ox bile and digestive enzymes earlier this year I was doing so still unclear as to exactly what was going on. I had pancreatitis symptoms and stool colour and digestion issues so I was covering all the bases with my approach.

Since I have had a CT scan and been told all looks fine, so I now know with the changes that it was cholestasis causing the issues so a reassessment of the regime would be pertinent. I have just sent a second stool sample for faecal elastase testing to check for lack of digestive enzymes from the pancreas.

The first must have been lost or something because I did everything correct, I was basically accused by the specialist of causing it not to be able to be done.

So I have taken photos of the label on the tube with form, stool and all and made a recording of me putting it in the drop box at the hospital. These will be sent in an email to them later or tomorrow just incase.

 

[anne_likes_red]

The only thing I could think of , is that those who have not removed their gallbladders (I have mine) , we do not need additional bile acids but instead we want to fix the composition of them ( and I believe TUDCA does that). Remember there exists lots of bile acids types.

@mariovitali I noticed in a previous post - which I can't find now! - that you were taking TUDCA (250mg?) at midday and midnight. Is the timing based on factors other than a 12 hourly dose? For example circadian liver processes...or a preference to take it away from other supplements?
Apologies if you've detailed this elsewhere and I've missed it.
I've used TUDCA sporadically but I'm wanting to give it a decent trial now I can get hold of it more easily.
Thanks, Anne.

 

[mariovitali]

@anne_likes_red What I do is take 750 mg daily, 250 mg every 8 hours (as I did not want to get one large single dose of 750 mg). Note that administration of UDCA suggests one single dose at bedtime :

Whereas levels of cholic acid and chenodeoxycholic acid (CDCA) decreased for the case of bedtime administration, this was not detected for mealtime administration, although no significant differences among the mean interval values were observed. A significant in difference decreased SI was observed during UDCA bedtime administration, but not during mealtime administration, compared to the SI before administration. This suggests a decreased cholesterol excretion into the bile. Based on these findings and from the point of view of compliance, bedtime administration of UDCA appears to be an effective method.

http://medical.med.tokushima-u.ac.jp/jmi/vol45/text/v45_n1-4_p115.html

So this is up to you