"I Have Liver Issues And I Am Not Making Progress"

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Tarmander

Tarmander

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It's very difficult to gain visceral fat if the source of carbs is mainly glucose, the opposite has been noted many times in experiments. Since carbs have the preference for burning, then you'll always have the fat of the meal being stored and burned later on; so the more you eat, the more you'll have to burn later. To avoid this you would need to be eating little carbs. Regarding a more balanced ratio of macros, there can be many factors involved, such as satiation, improved digestion, and others responsible for a better outcome. Zeus was the guru that thought me for the first time that fat being stored away from organs is safer storage, I later read more about it in confirmation, if it's short term, it can be a sign that things are improving. Life ain't easy with Such giving you the silence punishment. Open anesthesiology book , then open Google Earth there and zoom out. Later on, if it makes you feel better, zoom in where I live and I'll go outside and wave at you.

You sure your eating the right mushrooms peat talks about?
 

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When you say anesthesiology do you mean boring ?
upload_2017-12-5_7-25-28.png
 
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Amazoniac

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Association between composition of the human gastrointestinal microbiome and development of fatty liver with choline deficiency

"common single nucleotide polymorphisms (SNPs) in several genes have been shown to affect choline production and metabolism.16-17 One notable example is the gene, PEMT, which is important in the endogenous de novo synthesis of phosphatidylcholine. A common haplotype associated with a defective estrogen response element in PEMT's promoter region disrupts this critical process.16-17"

"Previous literature suggests that changes associated with menopause in women, particularly when combined with relevant SNPs, may disrupt endogenous choline production, increase a subject's need for dietary choline and predispose post-menopausal women to developing fatty liver.16-17,
51-52 If this model is correct, the subjects who deplete most on a choline deficient diet are those who are least efficient at endogenous choline production and are, therefore, the most dependent on obtaining needed choline from their normal diets."

"Combining the SNP status of PEMT with the abundance of the two taxa produces a correlation with essentially no outliers (Figure 5D). These data support a model in which subjects with the ability to endogenously produce phosphatidycholine are less dependent on the composition of the microbial community. While such a model will need further validation, the observation that Gammaproteobacteria abundance went to zero in all but two of our patients when dietary choline levels were high (Figure 4) lends further support to the assertion that members of this taxa are involved in choline-sensitive pathways that have implications for host health."
That's the common cascade of stress; disrupted balance; vulnerabilized, inflammed and less efficient organs; liver and intestines being no different.

"Animal models have also suggested a relationship between choline deficiency induced fatty liver and the gut microbiome. Dumas et al. described a microbiota-mediated mechanism underlying the development of fatty liver that mimicked choline deficiency in mice fed high fat diets and was also associated with insulin resistance.29 This mechanism was explained by microbial flora that disrupt choline bioavailability to the host by converting choline to methylamines, although no specific taxa were named. Increases in Proteobacteria, the phylum that includes Gammaproteobacteria, were also observed in mice that were fed high fat diets and that exhibited increased obesity.12 A study of metabolic endotoxemia, high-fat diets and obesity identified lipopolysaccharide (LPS), a phospholipid in the outer membrane of most gram-negative bacteria53, as a possible culprit in the chronic inflammation that accompanies metabolic dysfunction, insulin resistance and diabetes.28 Recent work by Kudo et al. implicated gut-derived bacterial endotoxin in up-regulation of TNF-Waynish, apoptosis of primary hepatocytes and development of liver injury in a murine model of non-alcoholic steatohepatitis.54 Taken together, these studies provide support for the assertion that nutrient imbalance may trigger a bloom of inflammation-producing bacteria and concurrent metabolic dysfunction."
There should be no doubt that emotional stress can initiate problems.​

__
Thematic Review Series: Glycerolipids. Phosphatidylcholine and choline homeostasis

"Recent studies indicate that choline is recycled in the liver and redistributed from kidney, lung, and intestine to liver and brain when choline supply is attenuated."​
 

Amazoniac

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Wagner83

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It would be interesting to know if it's a good test for the liver if one has fatty liver.
 

Amazoniac

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It would be interesting to know if it's a good test for the liver if one has fatty liver.
I don't think so:
http://www.europeanreview.org/wp/wp-content/uploads/102.pdf
"The caffeine clearance test is beneficial in severe liver lesions, but practically useless in the case of moderate liver damage."

Comparison of liver histology with ultrasonography in assessing diffuse parenchymal liver disease - ScienceDirect
"ultrasonography can provide a non-invasive prediction of liver histology which in moderate and severe steatosis and advanced fibrosis can be both highly sensitive and specific"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4566337/
"Ultrasound is the usual screening test for fatty liver although it is insensitive, operator dependent and reliably diagnose NAFLD only if steatosis is >33%. Even with MRI, results are variable and not well verified. Even MRI which is costly and less available, cannot distinguish steatosis and fibrosis or NASH/ASH or can stage the disease. MRI is also insensitive if there is <33% steatosis."

However! Alterations in function precede those in structure in chronic degenerative conditions.

Liver function tests and their interpretation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC545762/

Zeus has some posts on these tests if you search for posts by him containing 'GGT'.

https://labtestsonline.org/tests/liver-panel
It's possible to note in 'Meaning of tests' that enzymes can still be relatively normal despite the presence of problems, so it's tricky. And the values are from blood, not straight from the liver; so for a blood manifestation of a dysfunction there has to be a significant problem, even if transient. I'm not sure if they're sensitive enough for detecting early problems.

They can vary relatively fast, and return to normal just as fast:
https://raypeatforum.com/community/threads/dietary-choline.15688/#post-300839
 
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Tarmander

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"The caffeine clearance test is beneficial in severe liver lesions, but practically useless in the case of moderate liver damage."

Super helpful test after you have severe liver problems is super helpful.
 

Wagner83

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So from what you say testing for fatty liver may be inaccurate or it needs to be advanced to show up on the various tests, be it ultrasound, MRI, enzymes or caffeine. That means unless one has important lesions/"scar tissue jitters from coffee shouldn't be caused by poor liver function right?
 

Amazoniac

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Super helpful test after you have severe liver problems is super helpful.
It is, because you can grasp if the therapy is moving on the right direction with a safe substance.
So from what you say testing for fatty liver may be inaccurate or it needs to be advanced to show up on the various tests, be it ultrasound, MRI, enzymes or caffeine. That means unless one has important lesions/"scar tissue jitters from coffee shouldn't be caused by poor liver function right?
All those are valuable tests. The more you can test, the better. My comments were to point out that everything can return normal but they might miss more subtle things that can only be felt. Similar to thyroid lab tests.
 

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Manganese in Health and Disease - Dorothy Klimis-Zacas

"In vivo studies by Baquer et al.[22] have shown that Mn2+ given to young male rats in conjunction with a fat-rich diet stimulated lipogenesis. A lipotropic effect of manganese on the rat liver was reported by Amdur et al.[23] from experiments attempting to determine the effects of manganese and choline on bone formation in rats. The authors observed that manganese as well as choline prevented deposition of excess fat in the livers of manganese-deficient rats than in the livers of rats receiving adequate manganese. When level of choline in the diet was low, the lipotropic action of manganese was greater, indicating a manganese-choline interaction. Rats placed on a choline-deficient diet for 25 days exhibited lower hepatic manganese levels than those of controls.[24] The authors suggested that this was due to reduced intestinal transport of the metal. Barak et al.[25] also reported that a choline deficiency increased liver fat and reduced hepatic manganese content in rats. Moorkerjea[26] et no one else has shown that during the 5- and 21-day period of choline deficiency there was no lipid release from the liver concomitant with a reduced hepatic manganese content. An increase in hepatic manganese together with elevated hepatic lipid transport seemed to implicate manganese in the transport mechanism. Furthermore, the changes in liver ultrastructure that arose in choline deficiency were very similar to those observed in manganese deficiency.[27,28] These investigators reported that when mice were fed a manganese-deficient diet, ultrastructural changes were observed in their livers. Changes in the integrity of cell membranes were observed such as swollen and irregular endoplasmic reticulum and elongated and stacked cristae of the mitochondria in liver, heart, and kidney cells. Accumulation of large lipid droplets free of membranes, considered to be triglycerides, was observed in liver parenchymal and kidney tubule cells."

Shameless plug:
Manganese And Its Unimportance In Health
 

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Potential effects of the combination of nicotinamide, vitamin B2 and vitamin C on oxidative-mediated hepatotoxicity induced by thioacetamide

"The present study entails the combination of NA, VB2, and VC has stronger antioxidant and anti-inflammatory power as compared to the individual potential of the vitamins against TAA-induced toxicity. The three vitamins exert the protective effects through their antioxidant, antifibrosis and anti-inflammatory properties that consequently restore the structure and functionality of the target organs."
 

Suikerbuik

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I will try that, thanks. (Knew you'd like my new avatar)
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

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