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

[Broken man]

We cannot mention K2 without mentionning the problem for people having a tendency to clog.... I know some people can be killed by vitamine k2....
and what's its use for liver?
cafeine has to be detox by liver too.

Something with Kupfer´s cells in the liver. If you are interested, you can search for it. I had very high liver enzymes to the point that I was at hospital and gelatin, taurine, caffeine and vitamin K2 improved it.

 

[Xisca]

I don't know what my liver has appart what my organic acids test says and doctor said when I was a baby. And doctors do not say more than "liver". I was intoxicated by ethanol and propanol...
So I just say it is not ok to say that coffee is good for liver if not saying when and what for...
Is it good when you do not detox well? Is it good when you are not producing a lot of bile?

 

[Amazoniac]

Vitamin D and calcium, both have a direct suppressive effect on fat formation. The fatty liver for example, in animal studies it is corrected by both, vitamin D and calcium.

 

[Amazoniac]

https://www.westonaprice.org/health-topics/nonalcoholic-fatty-liver-disease/

"The discovery that choline could prevent the accumulation of fat in the liver was a byproduct of the seminal animal research conducted during the 1920s and 1930s showing that type-one diabetes was a disease of insulin deficiency. Physiologists first identified the role of insulin deficiency in type-one diabetes by studying the disease in dogs. In 1889 they produced diabetes by simply taking out the whole pancreas from these dogs and, after scrambling for a couple decades to identify the active component, they cured the diabetes with insulin in the early 1920s.75

Although cured of diabetes, the insulin-treated dogs nevertheless developed severe fatty liver degeneration and ultimately died of liver failure. Adding raw pancreas to their diet, which was composed of lean meat and sucrose, cured the problem. As researchers attempted to discover what it was in raw pancreas that cured the disease, they found in the early 1930s that egg yolk lecithin, which is abundant in choline, could cure it.76 Then they found that choline alone could cure it.77

It later turned out that the dogs became deficient in choline and methionine without a pancreas because they were not producing the digestive enzymes needed to free up those nutrients from the foods they were eating. Thus, simply providing them with the digestive enzyme trypsin could cure the fatty liver.78"

"In 1932 a group of researchers decided to replicate the fatty liver seen in the dogs in a nondiabetic rat model. What better way to stuff their livers with fat? Feed them fat! It seemed simple enough and it did indeed work. Although they had trouble reproducing the fatty liver with different colonies of rats or during the summer heat, they produced fatty liver in certain colonies of rats during the winter by replacing 40 percent of their ordinary cereal-based diet with beef drippings. Choline-rich lecithin derived from egg yolk or beef liver or simply choline itself cured the disease.79-80"

"virtually any form of energy delivered to the liver can cause the accumulation of fat, so long as key nutrients needed to metabolize that energy—such as choline—were missing."

"The initial experiments showing the protective effect of casein suggested that long-chain saturated fats might be more problematic than unsaturated fats or medium-chain fats (Figure 2a). As it turns out, saturated fats actually increase the need for choline slightly more than polyunsaturated fats (Figure 2b).85 Why this happens is unclear, but it may be that the body is quick to burn polyunsaturated fats for energy, since having them hang around is so dangerous. After all, if they hang around, they are likely to contribute to oxidative damage."

"There is some experimental evidence suggesting that polyunsaturated fats may impair the export of fats from the liver by facilitating oxidative damage of the proteins involved.86 This evidence comes from isolated cells and live animals injected with fatty acids. Substituting coconut oil for corn oil prevents steatosis in some,52 but not all,37 studies using choline-deficient diets. Polyunsaturated oils are probably most likely to contribute to the accumulation of liver fat when combined with other factors that favor oxidative stress such as alcohol abuse, iron overload, toxin exposure, and poor metabolism."

"Diets rich in fat or fructose will require more choline than diets rich in starch. Vitamin B6, folate, vitamin B12 and betaine (a nutrient found most abundantly in spinach and to a lesser extent in wheat and beets) all reduce the requirement for choline."

 

[Tarmander]

https://www.westonaprice.org/health-topics/nonalcoholic-fatty-liver-disease/

"The discovery that choline could prevent the accumulation of fat in the liver was a byproduct of the seminal animal research conducted during the 1920s and 1930s showing that type-one diabetes was a disease of insulin deficiency. Physiologists first identified the role of insulin deficiency in type-one diabetes by studying the disease in dogs. In 1889 they produced diabetes by simply taking out the whole pancreas from these dogs and, after scrambling for a couple decades to identify the active component, they cured the diabetes with insulin in the early 1920s.75

Although cured of diabetes, the insulin-treated dogs nevertheless developed severe fatty liver degeneration and ultimately died of liver failure. Adding raw pancreas to their diet, which was composed of lean meat and sucrose, cured the problem. As researchers attempted to discover what it was in raw pancreas that cured the disease, they found in the early 1930s that egg yolk lecithin, which is abundant in choline, could cure it.76 Then they found that choline alone could cure it.77

It later turned out that the dogs became deficient in choline and methionine without a pancreas because they were not producing the digestive enzymes needed to free up those nutrients from the foods they were eating. Thus, simply providing them with the digestive enzyme trypsin could cure the fatty liver.78"

"In 1932 a group of researchers decided to replicate the fatty liver seen in the dogs in a nondiabetic rat model. What better way to stuff their livers with fat? Feed them fat! It seemed simple enough and it did indeed work. Although they had trouble reproducing the fatty liver with different colonies of rats or during the summer heat, they produced fatty liver in certain colonies of rats during the winter by replacing 40 percent of their ordinary cereal-based diet with beef drippings. Choline-rich lecithin derived from egg yolk or beef liver or simply choline itself cured the disease.79-80"

"virtually any form of energy delivered to the liver can cause the accumulation of fat, so long as key nutrients needed to metabolize that energy—such as choline—were missing."

"The initial experiments showing the protective effect of casein suggested that long-chain saturated fats might be more problematic than unsaturated fats or medium-chain fats (Figure 2a). As it turns out, saturated fats actually increase the need for choline slightly more than polyunsaturated fats (Figure 2b).85 Why this happens is unclear, but it may be that the body is quick to burn polyunsaturated fats for energy, since having them hang around is so dangerous. After all, if they hang around, they are likely to contribute to oxidative damage."

"There is some experimental evidence suggesting that polyunsaturated fats may impair the export of fats from the liver by facilitating oxidative damage of the proteins involved.86 This evidence comes from isolated cells and live animals injected with fatty acids. Substituting coconut oil for corn oil prevents steatosis in some,52 but not all,37 studies using choline-deficient diets. Polyunsaturated oils are probably most likely to contribute to the accumulation of liver fat when combined with other factors that favor oxidative stress such as alcohol abuse, iron overload, toxin exposure, and poor metabolism."

"Diets rich in fat or fructose will require more choline than diets rich in starch. Vitamin B6, folate, vitamin B12 and betaine (a nutrient found most abundantly in spinach and to a lesser extent in wheat and beets) all reduce the requirement for choline."

Great quotes man. I have found that betaine HCL makes me feel awesome, so that last quote is interesting. Also, ate 7 eggs a day for a few months and got no reduction in visceral fat, which is a bit like a stand in for liver fat accumulation. So this choline thing is a bit questionable to me.

 

[Mito]

and got no reduction in visceral fat

How did you measure visceral fat?

 

[Amazoniac]

Great quotes man. I have found that betaine HCL makes me feel awesome, so that last quote is interesting. Also, ate 7 eggs a day for a few months and got no reduction in visceral fat, which is a bit like a stand in for liver fat accumulation. So this choline thing is a bit questionable to me.

Here's the problem that was mentioned a few pages back:
https://www.preprints.org/manuscript/201709.0040/v1/download
"Choline not only is an indispensable component of cell membrane phospholipids, but also plays important role in lipids metabolism. Choline facilitates the lipids transport in hepatocytes and prevents the abnormal accumulation of lipids in liver, while choline deficiency usually leads to hepatic steatosis [35, 36]. Gut microbiota also involve in choline metabolism by converting it into toxic dimethylamine and trimethylamine, which are transported to liver and converted into trimethylamine oxide (TMAO) that causes liver inflammation and damage [37]. The increased production of TMAO is also the culprit for cardiovascular disease [37-39]. On the other hand, the content of dietary choline influences the composition and abundance of gut microbiota that are associated with the development of NAFLD [40]. The close relationship between gut microbiota and choline metabolism provides important rationale for gut microbiota-targeted therapy for NAFLD.
Bile acids are synthesized from cholesterol with a wide range of physiological functions. Bile acids can not only facilitate digestion and absorption of fat-soluble food, but also preserve the intestinal barrier and preventing bacterial translocation [41, 42]. Moreover, bile acids could function as signaling molecules that modulate the balance of bile acids metabolism by activating farnesoid X receptor (FXR) and G protein-coupled receptor (TGR5)[43-46]. Study reveals that antibiotics could attenuate the high-fat diet-induced NAFLD development by altering the composition of bile acids and inhibiting FXR signaling pathway, whereas mice with intestine-specific Fxr disruption have reduced triglyceride accumulation in the liver compared with control mice [47]. Bile acids usually have strong anti-microbial property and gut microbiota can also influence the homeostasis of bile acids pool by deconjugating and metabolizing the primary bile acids into secondary bile acids in intestinal tract, which are involved in modulating lipids and energy metabolism pathways during NAFLD formation[44]. The crosstalk between gut microbiota and bile acids provides fundamental evidence for gut microbiota-targeted therapy of NAFLD."

Spoiler: Diagram

Spoiler: Baygons

"Compared to gut microbiota modulation with antibiotic, some ingredients from herbal medicines have shown effects on gut microbiota with minor side effects [152, 153]. Berberine is a typical herbal component with potent antibacterial activity, especially bacteria in intestinal tract because berberine can hardly be absorbed in gut [154]. Currently, increasing evidence has confirmed the therapeutic effect of berberine on metabolic diseases including obesity, NAFLD, and type 2 diabetes via modulation on gut microbiota [155-157]."

"TSG (2, 3, 5, 4’-tetrahydroxy-stilbene-2-O-β-D-glucoside) is an active component from Traditional Chinese Medicine (TCM) Polygonum multiflorum Thunb, which has shown significant effect on NAFLD prevention by modulating gut microbiota, improving the intestinal mucosal barrier and suppressing the expression of NF-κB [160]."

"Qushi Huayu Fang (a mixture of five herbs including Artemisia capillaries Thunb, Gardenia jasminoides Ellis, Fallopia japonica, Curcuma longa L., and Hypericum japonicum Thunb) is an ancient TCM formula which has been used for NAFLD treatment. Recent studies showed that administration of Qushi Huayu Decoction (QHD) significantly decreased body weight, alleviated hepatic steatosis, and reduced the content of TG and free fatty acids in liver in HFD-induced NAFLD rats. It showed that the CHF-treated group harbored significantly different gut microbiota from that of model rats, and the bacterial profiles of NAFLD rats could be modulated by the CHF [163, 164]. Recently, the anti-obesity property of daesiho-tang (DSHT) was also investigated. It was found that DSHT treatment significantly reduced serum TC and TG and hepatic fat accumulation which were associated with the regulation on abundance of gut microbiota [165]. Although the mechanisms underlying TCM are extremely complicated and largely unknown, gut microbiota was important target for many TCM formulas because many kinds of chemicals within TCM are unabsorbable that can influence gut microbiota directly or be metabolized into active form by gut microbiota."

In other words, it's not guaranteed, so once again cravings are more reliable.

 

[Amazoniac]

After reading Zeus' work in depth, I suspect that cheese omelettes are safer than plain eggs in that regard. Just a supposition because it's part of the Olympian diet.

 

[Amazoniac]

Cough. This discussion (TMAO) is not new, however it all depends on how you handle certain foods. And people with liver problems usually have chronic low-grade inflammation because of intestinal toxins.

 

[Tarmander]

Cough. This discussion (TMAO) is not new, however it all depends on how you handle certain foods. And people with liver problems usually have chronic low-grade inflammation because of intestinal toxins.

so if I understand you right, basically even people who are choline deficient, eating choline may just feed these bugs. Nice!

How did you measure visceral fat?

Nothing exact, just a fat percentage scale and looking at my stomach.

 

[Amazoniac]

No wonder we celebrate birthdays..

https://raypeatforum.com/community/quotes/99/

 

[Amazoniac]

https://www.researchgate.net/public...antethine_on_Fatty_Liver_and_Fat_Distribution

"Hypertriglyceridemia is divided into an exogenous type that increases chylomicrons and an endogenous type that increases very low density lipoprotein. The endogenous hypertriglyceridemia mainly results from excessive synthesis of triglycerides in the liver. Fatty liver develops when the amount of triglyceride synthesized in the liver exceeds that secreted from it. Therefore, the biochemical mechanisms of the two diseases overlap. Moreowa, fatty liver patients treated with pantethine showed not only improvement in the diseases, but also showed decreased visceral fat and increased subcutaneous fat. This indicates triglyceride may be pooled in the body as hepato-visceral fat and subcutaneous fat, and that pantethine may transfer fat from the liver and viscera to the subcutaneous tissue. This suggests that visceral fat deposition and fatty liver occurring with hypertriglyceridemia may have a common basis, probably excessive matrixes, and that pantethine may simultaneously improve the two conditions."

"In the present study, administering pantethine for six months quickly improved fatty liver."

Somewhat similar to the effects of niacinamide.

@EnerginConceiver

 

[haidut]

https://www.researchgate.net/public...antethine_on_Fatty_Liver_and_Fat_Distribution

"Hypertriglyceridemia is divided into an exogenous type that increases chylomicrons and an endogenous type that increases very low density lipoprotein. The endogenous hypertriglyceridemia mainly results from excessive synthesis of triglycerides in the liver. Fatty liver develops when the amount of triglyceride synthesized in the liver exceeds that secreted from it. Therefore, the biochemical mechanisms of the two diseases overlap. Moreowa, fatty liver patients treated with pantethine showed not only improvement in the diseases, but also showed decreased visceral fat and increased subcutaneous fat. This indicates triglyceride may be pooled in the body as hepato-visceral fat and subcutaneous fat, and that pantethine may transfer fat from the liver and viscera to the subcutaneous tissue. This suggests that visceral fat deposition and fatty liver occurring with hypertriglyceridemia may have a common basis, probably excessive matrixes, and that pantethine may simultaneously improve the two conditions."

"In the present study, administering pantethine for six months quickly improved fatty liver."

Somewhat similar to the effects of niacinamide.

@EnerginConceiver

I have no doubts that B5 is beneficial. The reason it is not in Energin is that I have not seen strong evidence that taken as supplement on top of what is in the diet will have benefit. And it is very hard to become B5 deficient these days as virtually all foods have been fortified with it.

 

[Amazoniac]

I have no doubts that B5 is beneficial. The reason it is not in Energin is that I have not seen strong evidence that taken as supplement on top of what is in the diet will have benefit. And it is very hard to become B5 deficient these days as virtually all foods have been fortified with it.

If what's available in the diet is enough, why would they notice an improvement when receiving supplements then?
This book discussed something related to the depleted state, which is: regular diet can only provide you enough to sustain health. Who knows what stress can do?
Also, what if it has a complementary action to the current others? You know I've been asking myself these questions for some time.
Most members don't eat fortified foods, especially burtlan because he's already fortified by nature.

--
All in all, it's something worth supplementing isolated from time to time to certify that we're getting enough.

 

[haidut]

If what's available in the diet is enough, why would they notice an improvement when receiving supplements then?
This book discussed something related to the depleted state, which is: regular diet can only provide you enough to sustain health. Who knows what stress can do?
Also, what if it has a complementary action to the current others? You know I've been asking myself these questions for some time.
Most members don't eat fortified foods, especially burtlan because he's already fortified by nature.

--
All in all, it's something worth supplementing isolated from time to time to certify that we're getting enough.

Fair enough, I will consider adding B5 to Energin.

 

[Tarmander]

If what's available in the diet is enough, why would they notice an improvement when receiving supplements then?
This book discussed something related to the depleted state, which is: regular diet can only provide you enough to sustain health. Who knows what stress can do?
Also, what if it has a complementary action to the current others? You know I've been asking myself these questions for some time.
Most members don't eat fortified foods, especially burtlan because he's already fortified by nature.

--
All in all, it's something worth supplementing isolated from time to time to certify that we're getting enough.

 

[Amazoniac]

Fair enough, I will consider adding B5 to Energin.

I'm actually more interested in reasons not to supplement it, I'm not selecting the positive evidence. This one in particular is concerning:
Hepatocellular Lipid Changes Produced by Pantothenic Acid Excess

However the majority I find is positive, even for liver:
STUDIES ON THE METABOLISM OF PANTOTHENIC ACID IN LIVER DAMAGE

From this link you can understand what led me to think about B5 again.
http://www.jbc.org/content/195/2/583.full.pdf

"after a certain stage in the deficiency is reached, so much damage has occurred to the adrenal gland that pantothenic acid cannot be immediately utilized."

"Administration of adrenal cortical extract enabled the deficient rats to raise their liver glycogen and blood sugar under anoxia as well as did the normal groups, strongly indicating that it is a lack of these hormones in pantothenic acid deficiency which produces the failure of carbohydrate metabolism under stress."

"That morphological damage occurs in the adrenal cortices of pantothenic acid-deficient rats has been well established (1, 3-6, 9). Our experiments demonstrate the deranged adrenal function produced by this deficiency, as evidenced by inability of the deficient rat to raise liver glycogen and blood sugar under anoxia. The deficient rats responded to anoxia as do adrenalectomized animals (19-22), but when given ACE [adrenal cortical extract] before the test period reverted to the normal. This is strong evidence in favor of the theory that pantothenic acid deficiency produces adrenal hypofunction."

"Apparently in riboflavin deficiency immediate repair of the carbohydrate mechanism can be effected if the vitamin is given, whereas in advanced pantothenic acid deficiency this ability has been lost. The fact that adrenal cortical extracts can instantly restore the mechanism in such animals points to the adrenal cortex as the site of the defect. Without pantothenic acid the gland appears to lose its ability to produce the gluconeogenic corticosteroids and to undergo structural changes not readily reparable."​

--
I find that studies such as this can be misleading.
https://www.jstage.jst.go.jp/article/jnsv1973/22/4/22_4_339/_pdf
They use healthy people for their experiments, but things might be different in sick people, or those that have chronic inflammation, fatigued, etc. An example would be the previous study, in which once exhaustion was reached, normalizing levels is way harder.
Studying nutrients that don't have clear external manifestations during deficiency is also more difficult. And even if it's hard to induce a deficiency, it doesn't mean that most people are on optimal amounts. Many things to consider((
People probably have enough reserves for 10 days, especially considering germ contribution. Yet they still notice negative effects (and these were healthy people). Check out the possibility of improving nitrogen balance by the end of the study.

https://www.jstage.jst.go.jp/article/jnsv/59/6/59_509/_pdf

 

[Amazoniac]

Zeus, check this out:

Pantothenic Acid: an Organ-Specific Pro-Oxidant Vitamin¶

"Coenzyme A is required for the initial activation of free fatty acids to fatty acyl-CoA thioesters prior to their oxidation or esterification to complex lipids 2,3. Consequently, it was expected that pantothenic acid deficiency would result in higher levels of free fatty acid in the liver, but not in the brain.
Surprisingly, however, analysis of tissue docosahexaenoic acid revealed that dietary pantothenic acid deficiency decreased the brain levels of this fatty acid by 30%, while virtually abolishing it in the liver (Fig 2). This finding can be explained based on the fact that pantothenic acid is also a structural element of the acyl carrier protein which is an essential component of the fatty acid synthetase complex 1."

"Pantothenic acid supplements to rats receiving pantothenic acid-deficient diet restored hepatic coenzyme A levels to control values (Fig 1), while increasing liver DHA levels by about 50%, supporting the conclusion that fatty acid synthesis is more susceptible to pantothenic acid than is its oxidation/esterification."

"In our study, brain and liver neuroprostane levels in control rats were 32+-4 ng/g and 29+-/4 ng/g, respectively (Fig 2). In parallel to the impact of pantothenic acid deficiency on tissue DHA, Pantothenic acid-deficient diet for 5 weeks did not change brain neuroprostane levels (Fig 2 ), while dramatically decreasing hepatic levels by 70% (Fig 2)."

"Similar to their effects on liver DHA concentrations, pantothenic acid supplements to these rats partially restored hepatic neuroprostane concentrations (Fig 2) ["Neuroprostanes result from free radical-induced peroxidation of DHA 5. This fatty acid is the most easily oxidizable naturally-occurring fatty acid"]. Whether or not longer duration of PA supplements to rats receiving PA-deficient diet would have completely restored hepatic DHA and neuroprostanes to control levels remains to be investigated.
These data show that dietary deficiency of PA has profound effects on hepatic coenzyme A and DHA levels, while exerting minimal or no effect on these metabolites in the brain. These organ-specific effects may be reflected in enhanced susceptibility of the liver to oxidative stress. This conclusion is evidenced by the diminished levels of neuroprostanes in livers of rats fed PA-deficient diet, coupled with undetectable changes in the brain levels of these sensitive markers of oxidative stress in the same rats."

"Animals and Diets
Male Sprague-Dawley rats (40-50 g; Sasco, Omaha, NE) were fed a PA-deficient diet (ICN Biomedicals, Costa Mesa, CA) for 5 weeks (PAD group), while control animals received regular rat chow for 5 weeks. Some rats receiving the PAD diet were supplemented with PA (100 mg/kg/d, orally) during the fifth week (PAD+PA group)."

However the majority I find is positive, even for liver

(((

 

[haidut]

Zeus, check this out:

Pantothenic Acid: an Organ-Specific Pro-Oxidant Vitamin¶

"Coenzyme A is required for the initial activation of free fatty acids to fatty acyl-CoA thioesters prior to their oxidation or esterification to complex lipids 2,3. Consequently, it was expected that pantothenic acid deficiency would result in higher levels of free fatty acid in the liver, but not in the brain.
Surprisingly, however, analysis of tissue docosahexaenoic acid revealed that dietary pantothenic acid deficiency decreased the brain levels of this fatty acid by 30%, while virtually abolishing it in the liver (Fig 2). This finding can be explained based on the fact that pantothenic acid is also a structural element of the acyl carrier protein which is an essential component of the fatty acid synthetase complex 1."

"Pantothenic acid supplements to rats receiving pantothenic acid-deficient diet restored hepatic coenzyme A levels to control values (Fig 1), while increasing liver DHA levels by about 50%, supporting the conclusion that fatty acid synthesis is more susceptible to pantothenic acid than is its oxidation/esterification."

"In our study, brain and liver neuroprostane levels in control rats were 32+-4 ng/g and 29+-/4 ng/g, respectively (Fig 2). In parallel to the impact of pantothenic acid deficiency on tissue DHA, Pantothenic acid-deficient diet for 5 weeks did not change brain neuroprostane levels (Fig 2 ), while dramatically decreasing hepatic levels by 70% (Fig 2)."

"Similar to their effects on liver DHA concentrations, pantothenic acid supplements to these rats partially restored hepatic neuroprostane concentrations (Fig 2) ["Neuroprostanes result from free radical-induced peroxidation of DHA 5. This fatty acid is the most easily oxidizable naturally-occurring fatty acid"]. Whether or not longer duration of PA supplements to rats receiving PA-deficient diet would have completely restored hepatic DHA and neuroprostanes to control levels remains to be investigated.
These data show that dietary deficiency of PA has profound effects on hepatic coenzyme A and DHA levels, while exerting minimal or no effect on these metabolites in the brain. These organ-specific effects may be reflected in enhanced susceptibility of the liver to oxidative stress. This conclusion is evidenced by the diminished levels of neuroprostanes in livers of rats fed PA-deficient diet, coupled with undetectable changes in the brain levels of these sensitive markers of oxidative stress in the same rats."

"Animals and Diets
Male Sprague-Dawley rats (40-50 g; Sasco, Omaha, NE) were fed a PA-deficient diet (ICN Biomedicals, Costa Mesa, CA) for 5 weeks (PAD group), while control animals received regular rat chow for 5 weeks. Some rats receiving the PAD diet were supplemented with PA (100 mg/kg/d, orally) during the fifth week (PAD+PA group)."


(((

Well, the fact that it increases fatty acid oxidation is not so good. This is probably why Peat does not write much about it and when I asked him he said "no need to supplement with B5 unless severely deficient".

 

[Amazoniac]

Time to include B5 antagonist in Energin.