Is there a liver connection in CFS/ME and have you been Tested?

Discussion in 'Fibromyalgia Main Forum' started by RadioFM, Mar 11, 2015.

  1. RadioFM

    RadioFM Active Member

    "Macrophage activation is a key event in the inflammatory process, since these cells produce a range of pro-inflammatory molecules, including ROS (reactive oxygen species), prostaglandins, cytokines and nitric oxide. These factors promote inflammation by causing vasodilation and recruitment of neutrophils, monocytes and lymphocytes, which ultimately clear infection and repair damaged tissue. One of the most potent macrophage activators is the Gram-negative-derived bacterial cell wall component LPS (lipopolysaccharide). LPS is sensed by TLR4 (Toll-like receptor 4) and triggers highly complex signalling pathways that culminate in activation of transcription factors such as NF-κB (nuclear factor κB), which in turn increases transcription of genes encoding proteins such as COX2 (cyclo-oxygenase 2, a key enzyme in prostaglandin biosynthesis), nitric oxide synthase and cytokines such as TNF (tumour necrosis factor). Recently, a role for metabolic pathways in the regulation of LPS signalling has become a focus of research in inflammation."

    "Although no mechanism is provided, the authors speculate that acetyl-CoA is synthesized from citrate in the cytosol. The acetyl-CoA generated could be required for phospholipid biosynthesis, the phospholipids being the source of arachidonic acid for prostaglandin production. Another product of citrate metabolism, oxaloacetate, will indirectly generate nitric oxide and ROS. This finding places citrate, transported from the mitochondria, as a key player in LPS signalling, at least for ROS, nitric oxide and prostaglandin production. This somewhat unexpected role for citrate in LPS action adds to a growing literature on the role for metabolism in the regulation of signalling in inflammation."
    Last edited: Mar 11, 2015
  2. RadioFM

    RadioFM Active Member

    "Many PWMEs are not able to convert pyruvate"

    "Pyruvic acid can be made from glucose through glycolysis, converted back to carbohydrates (such as glucose) via gluconeogenesis, or to fatty acids through acetyl-CoA. It can also be used to construct the amino acid alanine and be converted into ethanol."

    Rich Vanderburg has review many CFS/ME labs and has constantly seen low conversion of Pyruvate.

    • Could a Pyruvate deficiency lead to Acetyl CoA deficiency required for phospholipid biosynthesis be a contributing factor in CFS/ME?
    • Is there a liver connection in CFS/ME?
    • Would high does lipid exchange therapy be beneficial?

    Richvank QUOTE:

    " I think it is certainly possible to have low acetate in ME/CFS. Acetyl CoA is what feeds the Krebs cycle, and I have seen many urine organic acid panel results from PWMEs that are low in citric acid, which is the substance that acetyl CoA is converted into by the first reaction in the cycle. Many PWMEs are not able to convert pyruvate, from the glycolysis pathway, into acetyl CoA very well, judging from their test results. This conversion requires several of the B vitamins, magnesium, and lipoic acid."

    "So I think difficulty in making acetylcholine could be due either to low choline or low acetyl CoA, or both."

    Best regards,

    Last edited: Mar 11, 2015
  3. RadioFM

    RadioFM Active Member

    The endotoxin liver LPS-induced Kupffer cells connection?

    Many CFS/ME have elevated Alanine transaminase (ALT) WHY?

    Endotoxin and Kupffer Cell Activation in Alcoholic Liver Disease

    "As a result of endotoxin’s binding to CD14 and TLR4, Kupffer cells initiate various internal signaling processes. How endotoxin triggers these signaling pathways has been the subject of increasing research attention, given the importance of endotoxin and Kupffer cells in the development of alcohol–induced liver injury and other liver diseases."
    Last edited: Mar 11, 2015
  4. RadioFM

    RadioFM Active Member

    Last edited: Mar 11, 2015
  5. RadioFM

    RadioFM Active Member

    Is there a liver connection in CFS/ME?

    "Nonalcoholic steatohepatitis or NASH is a common, often “silent” liver disease. It resembles alcoholic liver disease, but occurs in people who drink little or no alcohol. The major feature in NASH is fat in the liver, along with inflammation and damage. Most people with NASH feel well and are not aware that they have a liver problem. Nevertheless, NASH can be severe and can lead to cirrhosis, in which the liver is permanently damaged and scarred and no longer able to work properly."

    See more below:

    The Silent liver disease.
  6. RadioFM

    RadioFM Active Member

    Liver Function Tests
    1. How is it used?
    2. When is it requested?
    3. What does the test result mean?
    4. Is there anything else I should know?

    How is it used?

    "Liver function tests are used to help determine the cause of symptoms such as jaundice that may be due to liver disease. They are also used to screen for potential liver damage, for example in alcoholics or people exposed to the hepatitis virus, and also to monitor changes in abnormal liver function."

    When is it requested?

    "These tests are used when symptoms suspicious of a liver condition are noticed. These include: jaundice, dark urine and light-coloured stools; nausea, vomiting and diarrhoea; loss of appetite; vomiting of blood; bloody or black stools; swelling or pain in the belly; unusual weight change; and fatigue or loss of stamina. One or more of these tests may be requested when a person has been or may have been exposed to a hepatitis virus; has a family history of liver disease; has excessive alcohol intake; or is taking a drug that can cause liver damage."

    What does the test result mean?

    "It is important to note that abnormal results in the individual tests can occur in conditions that do not involve the liver or the bile ducts and that, conversely, normal results can be found in patients with serious liver disease. However, one or more abnormal results often point to a diagnosis or to further investigations."

    • "Raised alanine aminotransferase (ALT) and aspartate aminotransferase (AST) values indicate leakage from cells due to inflammation or cell death. Liver disease is more likely when the values of AST and ALT are higher, ALT rising more than AST in acute liver damage such as hepatitis. When there is doubt about values, a raised creatine kinase (CK) will confirm muscle damage and measurement of troponin will show whether it is the heart that is damaged. Gamma-glutamyl transferase (GGT) seems to be more sensitive than ALT and AST for detecting liver damage from drugs and alcohol, and for detecting early rejection after liver transplantation."
    • "A raised total bilirubin is usually due to liver disease or blockage of the passage of bile to the gut, for example by gall stones. Bilirubin is made water soluble (conjugated) by the liver and is then excreted in the urine, the stools becoming pale. However, a raised bilirubin can also occur in conditions where the breakdown of red blood cells produces more unconjugated bilirubin than the liver can handle, for example in newborn babies. If this is suspected, both total and conjugated bilirubin are measured and monitored."
    • "Liver disease and blockage of the bile ducts also increase alkaline phosphatase (ALP). This is believed to be due to increased bile duct pressure causing the liver to make more ALP. If there are localised lesions within the liver, for example deposits of cancer cells, then ALP may be stimulated to rise but there may be sufficient normal liver around the deposits to keep bilirubin normal. Bone disease can also increase ALP. In patients with a normal bilirubin and a raised ALP, the measurement of 5’-nucleotidase (5’-NT) can help. It rises with liver ALP but is normal in bone disease."
    • "Albumin is made only in the liver and may be low when there has been extensive loss of liver tissue in long-standing disease. Other causes of a low albumin include malnutrition (which may accompany alcoholic liver disease), kidney disease, due to loss of protein in the urine, and inflammatory conditions anywhere in the body when the liver switches to making other proteins."
    • "Total protein is usually normal in liver disease. The difference between its concentration and that of albumin, called globulin, tends to increase when albumin falls, but very high values are seen most commonly in alcoholic hepatitis and in hepatitis caused by the body producing antibodies against its own liver (autoimmune hepatitis)."
    • "Patients with liver disease often bruise easily and cuts take a long time to stop bleeding. A long prothrombin time (PT) suggests a deficiency of clotting factors made by the liver or a deficiency of vitamin K which is needed for the factors to work. The deficiency can be the result of severe malnutrition, for example in alcoholism) or the result of blockage of bile passage to the gut. (Bile contains bile salts that are needed for the gut to absorb fat, and vitamin K is fat soluble.) Patients with a long PT may be given an injection of vitamin K and the PT measured again in 24 hours. A quicker PT after the injection indicates a deficiency of vitamin K rather than of clotting factors."

    Is there anything else I should know?

    "Depending on the history, examination and results of the liver function tests your doctor may request one or more further tests including alphafetoprotein, alpha-1 antitrypsin, CA 19-9, caeruloplasmin, copper, hepatitis virus antibodies A, B and C and smooth muscle antibody. Sometimes imaging scans are needed, and occasionally a small sample of liver is taken with a needle (biopsy) to be examined under a microscope."

    See more here:
    Last edited: Mar 11, 2015
  7. Willow77

    Willow77 Active Member

    Interesting. I have fatty liver. Diagnosed after a CT scan where my liver lit up like a Christmas tree. My doctor told me only treatment was to loose weight. I did lose weight and my alt went down to almost normal. But occasionally I get the pain in my liver area that led to the CT scan in the first place. I noticed on Web MD or some such site that it said to be careful with supplements with this disease so I was wondering how safe it is to do the ginger and cod liver oil juice? My Dr. doesn't like most supplements because there is no study to prove they are safe when taken in combination with the meds that I take. She okay-ed fish oil and the ginger is food but the other one for energy I don't know if it would be safe for me. The ginseng that was supposed to be so great for energy made me anxious and kept me awake all night. D-Ribose makes me feel weak and shakey. I am going to try just the ginger and fish oil. It isn't easy to find fresh ginger this time of year but in the summer I can get it very cheaply at the produce stand in the country. I may try freezing some juice in the summer for use in the winter as well as planting and growing it.

    I am excited to get started on this project as my HMO has no new ideas.
  8. RadioFM

    RadioFM Active Member

    Hey Willow,

    Do you have CFS or FM?
  9. Willow77

    Willow77 Active Member

    I think I had CFS first, then IC and then FMS about 5 years after onset.
  10. RadioFM

    RadioFM Active Member

    If you decide to not incorporate the NT Factor into the ginger recipe. You may never discover the true healing power of the Mitochondria to regenerate its self.

    The Lipid replacement therapy protocol has help me restore my Mitochondrial function and was essential part in regain my health.
    Last edited: Mar 12, 2015
  11. RadioFM

    RadioFM Active Member

    Ginger for Fatty Liver

    "An article published in the January 2011 issue of “World Journal of Gastroenterology” argues that ginger has great potential as a treatment for nonalcoholic fatty liver disease, or NAFLD, and emphasizes the need for research on the subject. This hypothesis is based on ginger’s antioxidant and triglyceride-lowering effects. Since oxidative stress is thought to be a primary cause of NAFLD, antioxidants like those in ginger may be able to prevent or reverse the disease. However, few well-designed clinical trials have been conducted to date. A 2008 study in the journal “Fitoterapia” reports that dietary ginger had significant antioxidant activity in rats with alcohol-damaged livers. However, there is no solid evidence that ginger affects alcoholic fatty liver disease in humans."

    See more here: