Isaiah 58:11
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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Sounds good in theory. But is it true? Morin is a flavonoid. If that can alleviate steatosis, surely it is possible a natural compound with the opposite effect can do harm.
https://www.ncbi.nlm.nih.gov/pubmed/28646531Our data reveal that morin is a dual antagonist of LXRα and LXRβ and suggest that morin may alleviate hepatic steatosis and other associated metabolic disorders via the suppression of LXR signalling and, therefore, shows promise as a novel therapy or nutraceutical for nonalcoholic fatty liver disease.
Albumin is synthesized in the liver, and low serum albumin may be indicative of liver failure or diseases such as cirrhosis or chronic hepatitis. Hypoalbuminemia can also present as part of the nephrotic syndrome, in which protein is lost in the urine due to kidney damage. Low albumin levels can be an indicator of chronic malnutrition or protein losing enteropathy.
An infectious disease specialist looked at my labs (high serum ferritin, AST, ALT) and pronounced that I had hepatitis... not A, B, or C, but something unspecified.I believe that we have some kind of Chronic Hepatitis / Inflammation of Liver that perpetuates a vicious cycle
When my daughter got MONO her liver enzymes shot through the roof due to liver inflammation. The EBV had attacked her liver. Her Dr. told me not to even think about giving her any Tylenol........not even 1 pill. I agree that infections can set up shop in the liver.My naturopath thinks one or more of my infections (c. pneumoniae, EBV, etc.) has set up shop in my liver.
A gastro/liver specialist said "that's ridiculous, no one has infections like that in their liver," and told me to stop taking supplements as they were causing liver inflammation and to get a colonoscopy.
Working the infectious angle and treating hemachromatosis has improved my labs to almost normal. And infections do tend to end up in the liver - just a few examples:
One example is methylation problems.The liver filters things from our blood and processes them using various chemicals. If its working hard at this, it can have a hard time keeping up and biochemical reserves can be depleted, causing a cascade of other biochemical problems which cause symptoms all over the body.
Thanks @mariovitali - good point. I actually have primary or hereditary hemachromatosis, which had been missed as it was milder due to being heterozygous for the 2 main HFE variants and not homozygous for the one.@Learner1
Secondary Hemochromatosis
Secondary hemochromatosis usually is the result of another disease or condition that causes iron overload. Examples of such diseases and conditions include:
- Certain types of anemia, such as thalassemias and sideroblastic anemia
- Atransferrinemia and aceruloplasminemia—both are rare, inherited diseases
- Chronic liver diseases, such as chronic hepatitis C infection, alcoholic liver disease, or nonalcoholic steatohepatitis
Yes, well that was why we investigated so thoroughly. Too much iron is indeed a bad thing. Your concern is warranted.@Learner1
I see. Please also be aware that high Iron can damage the Liver (due to Oxidative Stress).
So we could also make the hypothesis here that if Hemochromatosis has been left untreated for some time, it affected your Liver function (?)
Have you ever had a Fibroscan by any chance?
@mariovitali besides rapamycin, what are your thoughts on using TUDCA or coffee enemas to support the liver and LXR activation?
We have also shown that TD activates double-stranded RNA-activated protein kinase (PKR) which is also believed to play an important role in ER stress [97, 98]. These findings suggest that ER stress may underlie TD-induced damage to the CNS. To date, the mechanisms underlying TD-induced ER stress is unclear. It has been well documented that oxidative stress and disruption of calcium homeostasis can cause ER stress [99, 100].
These results suggest that autophagy is neuroprotective in response to TD-induced neurodegeneration in the CNS. There are several potential mechanisms for TD-induced autophagy. For example, TD is shown to affect mechanistic target of rapamycin (mTOR) and AMP- activated protein kinase (AMPK) pathways which are crit- ical regulators of autophagy [73]. Additionally, TD may activate autophagy through the induction of oxidative stress and/or ER stress because both oxidative stress and ER stress are known to stimulate autophagy
Fascinating. But we don't generally have all of the LXR related problems, do we? Atherosclerosis, diabetes, inflammation, and Alzheimer's disease. Well, inflammation for sure, but many possible causes of that.
For those who have 23andMe results, might be interesting to check for the LXR bad genes.
MAF of 22% is very high. And it's twice as high in those with European ancestry, at 44.4%. Expected genotype frequency is therefore 49% heterozygous and 19% homozygous. Your sample looks pretty average.I looked at the rs numbers you posted and on the DNA Samples i have (62 people with CFS, Post-Finasteride, Post-Accutane Syndrome) the most interesting appears to be rs2695121 having a MAF of 22%.