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

Amazoniac

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I will try that, thanks. (Knew you'd like my new avatar)
Admit that you just wanted me to look what you did with two hands. Turns out that I didn't like that specific avatar, it's silly and not in a good vvay. You think that you're being funny with that stick figure but in fact you're just using as an armour for your keyboard warriorness, you're being too ***** to upload your actual photo instead and stand behind your actions. The slopiness doesn't make you appear casual or carefree, it's obvious that it's forced and it contrasts with the many editions of your posts. Grow up and stop acting immature as if it had anything to do with actual youthfulness.

Yours,
Shoulder devil
 

Waynish

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Im interested to know what percentage of people on all these threads have fully regained their health or are doing significantly better?

Should make a poll. I noticed that based on various stories over the years that many people who "share" a lot seem to describe a health ailement that seems to me just as bad as they did in posts from years ago... Of course can't know their subjective experience, but then again most people can barely track their own subjective experiences.
 

Suikerbuik

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Jan 25, 2014
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Any follow-up on these patients where they gave them vitamin D to see if anything changed?
 

Amazoniac

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Any follow-up on these patients where they gave them vitamin D to see if anything changed?
Oh, great, you already changed your avatar. If people think that I was attacking you for no reason, I just want to clarify that it wasn't the case, I provided reasons. No mercy.

But I digest.

Anyway, I missed your message but I think you'll enjoy this:

[2] https://www.tandfonline.com/doi/full/10.1080/19381980.2016.1248325

"mediators induced by sun exposure other than vitamin D may play important roles in curtailing NAFLD"

"In light of the studies discussed in this review that found health outcomes related to sun exposure independent of vitamin D, health outcomes dependent on serum 25(OH)D levels but not vitamin D supplementation, and health outcomes dependent on mediators other than vitamin D, it is apparent that vitamin D supplements are not an effective substitute for adequate sun exposure."​
 
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Suikerbuik

Member
Joined
Jan 25, 2014
Messages
700
Oh, great, you already changed your avatar. If people think that I was attacking you for no reason, I just want to clarify that it wasn't the case, I provided reasons. No mercy.

But I digest.

Anyway, I missed your message but I think you'll enjoy this:

https://www.tandfonline.com/doi/full/10.1080/19381980.2016.1248325

"mediators induced by sun exposure other than vitamin D may play important roles in curtailing NAFLD"

"In light of the studies discussed in this review that found health outcomes related to sun exposure independent of vitamin D, health outcomes dependent on serum 25(OH)D levels but not vitamin D supplementation, and health outcomes dependent on mediators other than vitamin D, it is apparent that vitamin D supplements are not an effective substitute for adequate sun exposure."​

Yes I enjoy those studies. I see too many young people trying to correcting their vitamin D status by shots and pills, without vitamin A or other fat solubles.

Haha yes, of course I was not going to keep that picture. But I liked your reponse, no hard feelings. Btw I don't even know what to think of 'keyboard warriorness'.
 

Amazoniac

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Tony and Mike did a monstruous review. Read the publication for details. :ss

Plant-Based Foods as a Source of Lipotropes for Human Nutrition: A Survey of In Vivo Studies

"[..]lipotropes are defined as compounds that act on lipid metabolism by preventing fat accumulation within the liver by hastening fat removal or preventing excessive fat deposits (e.g., accumulation of TG and cholesterol)."

"Among PBF [plant-based foods], beetroot (Beta vulgaris), Chenopodiaceae-derived (e.g., spinach, lambsquarters, and whole-grain pseudocereals such as amaranth and quinoa) and Gramineae-derived (i.e., wholegrain cereals) plants are well recognized for their high betaine content, which is the result of an adaptation to environmental stress (Hanson and Hitz, 1982; Hanson and Wyse, 1982; Hitz et al., 1982; Hanson et al., 1985; Rhodes and Hanson, 1993; Yokoishi and Tanimoto, 1994; Craig, 2004; Ashraf and Foolad, 2007)."

"The lipotropic efficiency of betaine, choline, and myoinositol toward fatty liver has been demonstrated with lipotrope-deficient, high-fat/high-sucrose, or ethanol-enriched diets in rats (Supplemental Table 1; Halliday, 1938; Gavin and McHenry, 1940; Best et al., 1950; Chahl and Kratzing, 1966a; Hayashi et al., 1974a; Carroll and Williams, 1982; Barak et al., 1996a, 1996b, 1997). The efficiency was determined through dose-response curves. Choline had three-fold the potency of betaine and methionine, and betaine is more efficient than myo-inositol."

"[..]in 1954, Nadeau et al. suggested that fatty liver in alcoholic patients may result from a dietary deficiency that leads to choline deficiency, and they observed that the administration of lipotrope tablets led to rapid improvement of hepatic function. This was determined by noting the decreasing values of the bromosulfalein test; this test has been shown in dogs to be closely related to hepatic fatty overload (Hough et al., 1943; Popper and Schaffner, 1952). These lipotrope tablets were seen as a significant supplement to an adequate diet (Nadeau et al., 1954). In 1964, several authors reported improvements of hepatic function and atherosclerotic markers in humans with hepatic and/or cardiovascular dysfunctions following administration of Ornitaine(R) (10.045 formula, Jacques Logeais Laboratory, Issy- Les-Moulineaux), a cocktail containing ornithine chlorhydrate and other associated substances such as pyridoxine chlorhydrate, sorbitol and two lipotropes—betaine and magnesium citrate (Navarranne et al., 1964; Warembourg and Bertrand, 1964). In 1991, Zeisel et al. reported that within three weeks, choline-deficient subjects developed symptoms of incipient liver dysfunction, notably an increase in serum alanin aminotransferase (ALT) and a decrease in plasma phosphatidylcholine (Zeisel et al., 1991)."

"In 2005, patients with NASH were shown to have their biochemical and liver histology parameters improved (notably decreased grade of inflammation and stage of fibrosis) following one year of treatment with betaine anhydrous (10 g twice a day; Mukherjee et al., 2005; see also Supplemental Table 1 for details). More recently, men (40% of the 20 tested) and postmenopausal women (80% of the 15 tested) deprived of dietary choline have been reported to develop hepatic steatosis, the most common sign of choline deficiency (Fischer et al., 2007)."

"Eight weeks of oral betaine glucuronate combined with diethanolamine glucuronate (used for PL synthesis) and nicotinamide ascorbate significantly reduced hepatic steatosis scores and liver enlargement without adverse effects in patients with NASH compared to a placebo (Miglio et al., 2000)."

"Concerning myo-inositol, we found no human studies directly dealing with its effect on liver steatosis or lipid metabolism. However, several studies conducted around 1950 showed serum lipid biomarker improvement—notably a decreased level of cholesterolemia—following myo-inositol administration (1–3 g/day) for several weeks in both diabetics and patients with disorders of lipid metabolism (Felch and Dotti, 1949; Leinwand and Moore, 1949; Gargini, 1951; Felch et al., 1952; see also Supplemental Table 1)." "Because myo-inositol is not a methyl donor, its lipotropic effect is mainly based on its ability to favor phosphatidyl inositol synthesis that is thereafter used for lipoprotein formation in the endoplasmic reticulum or for lipoprotein transport from the liver to the bloodstream (Figure 2A; Yagi and Kotaki, 1969)."

"The lipotropic effect of methionine was demonstrated to be based on the methyl supply for choline synthesis (see Figure 2A; du Vigneaud et al., 1940, 1941). It was later confirmed that methionine does not directly act upon lipid metabolism but rather that it acts as a precursor of choline through methyl donation to phosphatidylethanolamine (Figure 2A; Labadie, 1974). Its lipotropic potency would be weaker than that of choline at equivalent quantities (Chahl and Kratzing, 1966b), up to three-fold lower, as shown in young rats (Griffith and Mulford, 1941a)."

"Phosphatidylcholine is indispensable for exporting fat outside hepatocytes, and methionine indirectly contributes to fat exportation from the liver by facilitating the formation of choline."

"[..]the impairment of lipoprotein and TG secretions from the liver, the subsequent increase in hepatic TG synthesis (i.e., increased activity of FAS; Rosenfeld, 1973), and the decreased plasma PL levels (lecithins and sphingomyelins) of chilomicrons, VLDL, and LDL have been reported in rats deprived of choline (Olson et al., 1958a; Lombardi et al., 1968; Mookerjea, 1971; Mookerjea et al., 1975). TGs are characterized by increased palmitic acid (16:0) content (Rosenfeld, 1973)—the latter was the first FA produced during lipogenesis and from which longer FA are generated. In the absence of adequate phosphatidylcholine, cholesterol and TG are likely to move toward cytosol, leading to a fatty liver, as shown in choline-deficient rats (da Costa et al., 1995). In choline-deficient rats, Yao and Vance (1990) observed hepatic TG accumulation, plasmatic TG and VLDL reduction, a decrease in phosphatidylcholine, and a TG content of VLDL but no change in the plasmatic HDL level."

"In the end, another unexpected—but hypothetic—cellular mechanism might be involved in the lipotropic effect of betaine, choline, and myo-inositol. Indeed, as small hydrosoluble molecules that do not interfere with cellular protein functions—even at high concentrations—betaine, choline, and myo-inositol are all osmolytes and may participate in cell volume regulation, with the level of cellular hydration affecting cellular metabolism via gene expression modifications (Häussinger, 1996). Thus, increased cell swelling in rat hepatocytes was shown to increase lipogenesis and activate ACC (Baquet et al., 1991; Hue, 1994). This enzyme allows formation of the metabolic intermediate malonyl-CoA that plays a major role in FA synthesis."

..
"Lipotrope-deficient diets may be carcinogenic in the absence of carcinogens (Poirier and Whitehead, 1973; Henning and Swendseid, 1996; Moon et al., 1998)."

"[..]a decrease in the amount of methyl groups [available] within an organism would favor an increased susceptibility toward cancers by altering immune function and xenobiotic (e.g., carcinogen) metabolism (Nauss et al., 1982; Newberne and Rogers, 1986)."

"The lipotrope/methyl donor-deficient diet is therefore the only dietary deficiency to be carcinogenic (Ghoshal and Farber, 1984; Locker et al., 1986). Perhaps this is one of the reasons why both lipotrope- and methyl donor deficiencies have been, purposely or not, often confounded until now. However, as shown by a simple database interrogation, the term methyl donor-deficient diet is more often used today than lipotrope-deficient diet. Yet, while all lipotropes are not methyl donors (e.g., myo-inositol and betaine), all methyl donors have not been shown to be lipotropic (e.g., S-adenosyl-methionine)."

"Based on the previously demonstrated lipotropic effect of betaine and choline (Best and Huntsman, 1932), it was hypothesized that amino acids from casein were converted into betaine and choline in the liver (Channon and Wilkinson, 1935). Determining which amino acid was most involved in the lipotropic effect of proteins led researchers to show that methionine was lipotropic and that 0.5% cystine supplementation in the diet increased the fatty liver content in rats (Beeston and Channon, 1936; Tucker and Eckstein, 1937). Lysine had no effect (Tucker and Eckstein, 1938). In addition to the lipotropic effect of methionine from casein, that of threonine was also suggested (Beveridge et al., 1945) and then confirmed (Harper et al., 1953), but it partly depended on the amount of tryptophan, glycine, or protein in the diet (Singal et al., 1953; Harper et al., 1954b). A small lipotropic effect of tryptophan and of glutamic acid—but only with a high-cholesterol liver, not with a high-FA liver—was otherwise reported (Channon et al., 1943). Except for methionine, a lack of lipotropic effect for all other essential amino acids, including threonine, was also observed in rats (Eckstein, 1952)."

"A series of proteins was also tested for their lipotropic activity, and the following ranking was obtained, listed in order of deceasing intensity: gromax and whale muscle protein > caseinogen > albumin > beef muscle protein and edestin > fibrin and gliadin > gelatin and zein (Channon et al., 1938). The lipotropic effect of these proteins correlated with their methionine content (Tucker and Eckstein, 1938). Thus, arachin, a protein of low methionine content, had no lipotropic activity (Singal and Eckstein, 1939)."

"In 1969, it was demonstrated that rats fed a low-protein diet (5% casein only) had a higher hepatic total FA content compared to a normal diet and a lower level of liver PL (27%) after six weeks (Osumi et al., 1969). The lipotropic action of proteins was further underlined in rats and woodchucks, for which the effect of lipotropic factors (choline, methionine, folic acid, and vitamin B12) varied according to the amount of soy protein isolate in the diet (i.e., 10 vs. 20%; Boyd et al., 1986)."

"[..]hydrophobic peptides of soybean protein bind bile acids and consequently stimulate hepatic cholesterol turnover (Iwami et al., 1986). Moreover, in rats highly purified soybean proteins affect enzymes involved in cholesterol metabolism (Madani et al., 1998)."

"In humans, the lipotropic effect of proteins has apparently not been studied in depth. A report was made of a mildly hypercholesterolemic and healthy middle-aged alcoholic woman on either a normal diet containing 100 g protein or a low-protein diet of 25 g: liver biopsies did not reveal any fatty material accumulation while on the low-protein diet but important decreases in lipid (cholesterol, PLs, and TGs) and lipoprotein concentrations were observed in the serum, suggesting impairment of lipid metabolism within the liver, most notably for cholesterol (Olson et al., 1958b). The administration of a supplement of lipotropic factors (choline, methionine, inositol, vitamin B12, and liver concentrate) restored the serum cholesterol to its normal level (Olson et al., 1958b)."
This is interesting. The blood levels can decrease in proportion to the accumulation.

"Myo-inositol is present in PBF mainly in its free or conjugated forms, such as galactinol (i.e., monoglycosylated myo-inositol), di-glycosylated myo-inositol (Sosulski et al., 1982; Horbowicz et al., 1998; Steadman et al., 2000), or myo-inositol phosphates such as myo-inositol hexakisphosphate (i.e., IP6) or phytic acid, which is generally the most abundant myo-inositol phosphate followed by IP5, IP4, and so forth (Chen, 2004; Helfrich and Bettmer, 2004). However, regarding the high phytic acid content in numerous PBF, especially grain products—i.e., whole-grain cereals, legumes, nuts, and seeds—the question of whether phytic acid has to be considered as a source of lipotropes is an important issue." "[However,] the extrapolation of the lipotropic effect of myo-inositol phosphates from rats to human remains highly uncertain and premature."

"[..]in rats fed a 20% protein and choline deficient diet, carnitine surprisingly did not prevent fatty liver, whereas choline did, probably because the methyl group of carnitine is not labile and cannot be transferred to form methionine from homocysteine (Fritz and Dupont, 1957)."

"Carnitine found in the body is produced by synthesis from dietary lysine and methionine (Figure 2C) and from natural carnitine found in low amounts in PBF such as avocado, tempeh (fermented soya), some nuts, seeds, legumes, vegetables, fruits, and cereals (e.g., pumpkin, sunflower, sesame, cabbage, common bean, apricots, and banana). Compared to animal tissues, the carnitine and acylcarnitine (2% of the total carnitine pool) contents in plant tissues are around one hundred and one thousand times lower, respectively (Bourdin et al., 2007). The best sources are of animal origin, such as red meat and, to a lesser extent, milk products (Seline and Johein, 2007). Values of 0.32, 0.51, and 0.27 mg/100 g dry weight (dw) have been reported for rapeseed, flax, and tobacco, respectively (Bourdin et al., 2007). These values are closer to the ranges of B vitamins in PBF than those found for betaine, choline, myo-inositol, and methionine."

"Among PBF, mushrooms (1.32, 2.62, and 4.98 mg/100 g for chanterelles, “mushroom,” and oyster mushrooms, respectively) appear to be the best source of carnitine, both on a 100 g fresh food and on a dry weight basis"

"In addition to the well-recognized lipotrope compounds—choline, myo-inositol, methionine, and betaine—the contribution of micronutrients such as niacin (vitamin B3; Perry, 1960; van der Hoorn et al., 2008), pantothenic acid (vitamin B5; Catolla Cavalcanti and Levis, 1950; Turchetto et al., 1955), folate (vitamin B9; Kelley et al., 1950; Laird and Drill, 1971), and magnesium (Colson and Gallay, 1964; Navarranne et al., 1964;Warembourg and Bertrand, 1964) to the overall lipotropic effect of PBF has also been emphasized (Supplemental Table 1). Although it was shown very early on to exert a lipotropic effect in rats (Halliday, 1938), pyridoxin (vitamin B6) is no longer considered a lipotrope (Carter and Phizackerley, 1951) because of further contradictory results (Gavin and McHenry, 1940; McHenry and Gavin, 1941; Johnston et al., 1961; Saheb and Demers, 1972; Audet and Lupien, 1974). The lipotropic effect of pyridoxin has not been convincingly confirmed, despite several studies showing the development of fatty liver in rats fed a high protein diet without pyridoxin (Okada and Ochi, 1971; Okada and Suzuki, 1974; Suzuki et al., 1976; Abe and Kishino, 1982). Therefore, although some have considered it to be a lipotrope and although it is used in commercial lipotrope supplements, the literature does not contain enough convincing data to validate it as a lipotrope, especially in humans."

"The lipotropic effect has also been reported for vitamin B12 (cobalamine) either alone (Drill, 1954; Shils and Stewart, 1954; St. Greif and Wenning, 1954; Quan and Le Breton, 1973) or in combination with choline and folates (Laird and Drill, 1971)."

"The mechanisms by which magnesium and B vitamins may limit fat deposits are multifactorial, especially for niacin."

"For folates (or folic acid), the mechanism involved in its contribution to the overall lipotropic effect is its action as a precursor of the methyl donor 5-methyl tetrahydrofolate that leads to methionine formation from homocysteine via methyl donation and later to choline regeneration (Figure 2A; Zeisel, 1981)." "[..]it appears to be effective only when adequate amounts of other lipotropes, notably choline, are initially present in the diet (Laird et al., 1965). In addition, rats fed a folate-depleted diet had their hepatic choline and phosphocholine concentrations decreased by ∼67% and ∼78%, respectively (Kim et al., 1994). The supportive lipotropic effect of folates is concomitant with their ability to reduce hyperhomocysteinemia (Brouwer et al., 1999; Moat et al., 2003), a CVD risk factor."

"[..]the potentiated hepatic steatosis induced by high doses of nicotinic acid [] may be ascribed to its interference in the transmethylation process by preventing methionine from providing methyl groups for choline synthesis and by blocking vitamin B12 from acting as a co-factor in the methylation of homocysteine in methionine (Rikans et al., 1964; Baker et al., 1977). Accordingly, it had previously been hypothesized that the antilipotropic effect of nicotinic acid at high doses (from 1% to 4%) might be due to the important need for methyl groups by its detoxification products (Schön, 1958). Most notably, nicotinamide requires more methyl groups for excretion than nicotinic acid (Miller et al., 1960), and excess niacin is methylated in the liver to N-methyl-nicotinamide and then excreted in the urine (Institute of Medicine and Food and Nutrition Board, 1998). This causes nicotinic acid to assimilate to a “methyl trap that drains off methyl groups from choline and/or methionine synthesis, leading to a functional choline deficiency” and leading to impaired secretion of lipids from the liver (Perlzweig et al., 1943; Handler, 1944; Cantoni, 1951; Baker et al., 1977). Indeed, addition of choline generally reverses the fatty liver induced by excess niacin (Rikans et al., 1965; Baker et al., 1977)."

"Nicotinic acid has been shown by different authors to significantly reduce the liver cholesterol contents and its rate of biosynthesis (Merrill and Lemley-Stone, 1957; Schön, 1958; Schade and Saltman, 1959; Perry, 1960), an effect attributed to a lack of acetyl-CoA, which is needed for cholesterol synthesis, CoA competing with detoxication systems—notably towards nicotinuric acid at high doses of nicotinic acid—and lipid synthesis (Schade and Saltman, 1959). Other authors advanced the idea that nicotinic acid would divert cholesterol precursors toward oxidation rather than toward the cholesterol synthesis pathway, as occurs with FA formation (Perry, 1960)."

"Actually, other mechanisms might be involved in the reported positive effect of niacin on hepatic lipid metabolism. In vitro, at various doses, nicotinic acid has been shown to significantly inhibit (from 19% to 100% for 10 to 100 μmoles of nicotinic acid, respectively) ACC activity, the main enzyme involved in FA synthesis (Fomenko et al., 1979). Yet, with the objective of unraveling the mechanisms by which nicotinic acid inhibits ketogenesis, Yeh incubated in vitro mitochondria with palmitic acid, CoA, carnitine, and nicotinic acid and showed that nicotinic acid had no influence on the rate of β-oxidation, suggesting that the enzymes required for palmitate β-oxidation and the production of acetyl CoA are not affected by nicotinic acid (Yeh, 1976). This would confirm previous results showing a lack of effect of nicotinic acid on the hepatic acetyl-CoA concentration at an injection level of 50 mg/kg body weight (Mayor et al., 1967). Based on the antioxidant property of copper (Cu) and on the hypolipidemic capacity of niacin, Salama et al. interestingly demonstrated in high-carbohydrate fed rats that a copper nicotinic acid complex (a therapeutic drug) administered by stomach tubing at apparently nutritional doses—i.e., 400 mg/kg—is able to correct fatty liver by significantly decreasing the total lipid content and increasing the antioxidant status (Salama et al., 2007). Increased oxidative stress via accumulation of free radicals may lead to fatty liver. Indeed, a decreased expression of superoxide dismutase has been observed in patients with cirrhotic stage NASH (Sreekumar et al., 2001). Such a decrease generally leads to increased levels of reactive oxygen species (ROS) that may yield mutations in mitochondrial DNA; the mitochondria are the site of FA β-oxidation (Sreekumar et al., 2001). Finally, niacin, together with pyridoxin, vitamin C, iron, and other enzymes, participates in the synthesis of the lipotrope carnitine (Figure 2C)."

"[..]niacin may
(1) inhibit TG production and FA synthesis combined with accelerated ApoB (a TG-rich lipoprotein) degradation (Kashyap et al., 1997; Jin et al., 1999; van der Hoorn et al., 2008);
(2) increase the efflux of HDL ApoA-1 (Jin et al., 1997);
(3) reduce intracellular cholesterol (total, free, and esters; van der Hoorn et al., 2008);
(4) induce expression of PPARα mRNA (PPARα regulates FA oxidation and stimulates peroxysome proliferation; Siripurkpong and Na-Bangehang, 2009);
(5) up-regulate ATP-binding cassette transporter 1 (ABCA1) mRNA expression (Siripurkpong and Na-Bangehang, 2009)—ABCA1 effluxes excess cellular cholesterol to ApoA-1 to form nascent HDL;
(6) reduce expression of cholesteryl ester transfer protein (CETP)mRNA(van der Hoorn et al., 2008)–-CETP mediates the transfer of cholesteryl
esters from HDL to proatherogenic apoB-lipoproteins;
(7) inhibit hepatocyte diacylglycerol acyltransferase (DGAT), the key enzyme for the synthesis of TGs, finally resulting in a potential reduction of hepatic atherogenic lipoprotein secretion (Ganji et al., 2002);
(8) inhibit surface expression of the ATP synthase β chain—the latter mediates hepatic HDL endocytosis (Martinez et al., 2003); and, consequently,
(9) reduce HDL uptake by HepG2 cells (Zhang et al., 2008)."

"Recently, lower doses of niacin, up to 50.1 mg daily, have been tested in healthy volunteers, and it has been observed that a 16.7 mg-dose of niacin does not cause flushing symptoms but that they occur sporadically at a 50.1 mg dose (Schweikart et al., 2009). In addition, no change occurred in the blood pressure, pulse, and skin temperature of the volunteers (Schweikart et al., 2009). Niacin may also reduce the release of FFAs in plasma through inhibition of catecholamine stimulation of TG lipolysis in adipose tissue (Arner, 1999), as shown in vitro (Carlson, 1963), leading to reduction of hepatic VLDL-TG production (Figge et al., 1988; Chapman et al., 2010) and resulting in decreased plasma VLDL-TG concentrations (Grundy et al., 1981)."

"Compared to other lipotropes, the physiological mechanisms involved in the supportive lipotropic effect of niacin therefore appear to be multifactorial and dependent on the presence of other lipotropes (i.e., a potential synergetic lipotropic effect) and on the dose used (Figure 2C and Supplemental Table 1)."

"As with niacin, apparently contradictory results have also been reported for pantothenic acid (Griffith and Mulford, 1941b; Schaefer et al., 1942; Morgan and Lewis, 1953; Carter and Hockaday, 1962)."

"[..]it was found that feeding rats with a B vitamin-deficient (including thiamine, riboflavin, pantothenic acid, and pyridoxine) or a pantothenic acid-deficient diet prevented the development of fatty liver (Engel, 1942; Morgan and Lewis, 1953), notably an increased cholesterol content in high-cholesterol-fed rats (Guehring et al., 1952), pantothenic acid being indirectly involved in the transformation of acetate into cholesterol (Bloch and Rittenberg, 1942) via acetyl-CoA action and being constitutive of the coenzyme."

"[..]αdrenal hormone [is] synthesized from cholesterol and pantothenic acid [is] involved in cholesterol synthesis (Morgan and Lewis, 1953)."

"[..]such results emphasized the different effects of pantothenic acid on hepatic lipid metabolism (see Supplemental Table 1). We believe that the contradictory results obtained with both niacin and pantothenic acid probably depend not only on the presence or absence of the other main lipotropes—choline, betaine, methionine, and myo-inositol—or other B vitamins, but also on the doses, on the animal species used, and on the experimental scheme. In other words, the lipotropic action of B vitamins, notably niacin and pantothenic acid, is probably exerted in synergy with other lipotropes. This is the reason why, in the end, we have assumed that niacin and pantothenic acid indirectly support and contribute to the overall lipotropic effect of PBF under normal dietary conditions, i.e., at normal doses and in the presence of other lipotropes. Accordingly, pantothenic acid is commonly used today in lipotropic supplements."

"The depletion of magnesium has been associated with cirrhosis (Koivisto et al., 2002), and hypomagnesemia has been associated with NAFLD and NASH (Hanje et al., 2006). A low plasma level of magnesium has also been associated with insulin resistance (Rosolova et al., 1997), and a low magnesium diet was shown to decrease insulin sensitivity (Nadler et al., 1993). Magnesium has also been shown to reduce hyperlipidemia (Kisters et al., 1993).

More specifically, magnesium is well known as an antioxidant (Freedman et al., 1992). It is also particularly involved in the reaction of CoA with ATP (Mg-ATP complex) and FFA to yield acyl-CoA (Figure 2B), and it activates CoA synthesis from pantothenic acid proportionally to the presence of ATP. It is also required by mitochondria for oxidative phosphorylations that produce ATP. All of these properties of magnesium play a role in the overall FA β-oxidation process (Figure 2B; Ingraham and Green, 1958; Berg, 1959; Andrieux-Domont and Le van, 1970; Garfinkel and Garfinkel, 1985). The role of magnesium in FA oxidation was well illustrated by the dramatic increase of palmitate oxidation reached in heart muscle mitochondria when the magnesium concentration was increased from 0.01 mM to 5 mMin the presence of carnitine (≈+800%) or acetylcarnitine (≈+950%; Supplemental Table 1; Fritz, 1959).

Regarding these specific properties of magnesium and because increased oxidative stress and insulin resistance may be associated with fatty liver, magnesium may be considered to indirectly support and contribute to the overall lipotropic effect of PBF. It has been cited as a lipotrope in the clinical report of Colson and Gallay (Colson and Gallay, 1964) and is commonly used as such in current commercial lipotrope complexes. There are, however, no human studies investigating the effects of magnesium therapy in patients with a fatty liver."

They discuss hydroxycitric acid as useful but I'm not familiar with it, so I don't know if it's worth spending time reading about it.

"Water-soluble (e.g., s-allyl cysteine, s-ethyl cysteine, n-acetyl cysteine, and s-propyl cysteine) and lipid-soluble (e.g., diallyl sulfide and dipropyl sulfide) organosulfur compounds have been shown in mice or rats fed a methionine-choline deficient (Lin et al., 2008), high-fat (Lin and Yin, 2008), or high-cholesterol (Kumari and Augusti, 2007) diet to alleviate and/or to protect the liver from induced hepatotoxicity and from high saturated fat-associated oxidative damages. They also reduce the hepatic biosynthesis of TG and cholesterol (Supplemental Table 2; Lin et al., 2004; Kumari and Augusti, 2007). Similar results were reported in diabetic mice (Hsu et al., 2004). Some of the mechanisms involved—notably uncovered using rat hepatocytes—are probably related to the decreased activity of two lipogenic enzymes (ME and FAS), the decreased activity of HMG-CoA reductase, and the reduced rate of acetate ormevalonate incorporation into lipids (Supplemental Table 2; Yeh and Yeh, 1994; Kumari et al., 1995; Gebhardt and Beck, 1996; Liu and Yeh, 2000; Lin et al., 2004; Kumari and Augusti, 2007; Lin and Yin, 2008; Lin et al., 2008)."

"[..]results convincingly support the presence of a lipotropic effect for organosulfur compounds."

Hopefully burltan is still here.

"The only human studies concern patients with NAFLD who were administered 0.8–2 g daily of PUFA for 6–12 months (Capanni et al., 2006; Spadaro et al., 2008; Sofi et al., 2010). The results clearly showed a significant decrease in the degree of steatosis, with 17–30% of subjects having no more steatosis diagnosed (Capanni et al., 2006; Spadaro et al., 2008; Sofi et al., 2010). However, the PUFA were either of animal origin (Capanni et al., 2006; Sofi et al., 2010) or no precise origins were given (Spadaro et al., 2008)."
?
If someone reads them, let me know how they were done?

"The fact that Japanese men consuming the highest amounts of n-3 PUFA in the form of EPA ± DHA have the lowest prevalence of NAFLD (Oya et al., 2010) might further support the use of these n-3 PUFA as lipotropic agents. A marked enhancement in the long-chain PUFA n−6/n−3 ratio has been observed in the livers of NAFLD patients. Such a condition is likely to “favour lipid synthesis over oxidation and secretion, thereby leading to steatosis (Araya et al., 2004, p. 635)."

"While olive oil consumption significantly reduced the hepatic TG content by around 29%, fish pboyl consumption did not (Supplemental Table 5; Hussein et al., 2007). Accordingly, the role of the oleic acid in olive oil in preventing steatosis in NAFLD patients has been later discussed (Assy et al., 2009). Indeed, oleic acid is able to decrease NF-κB activation and LDL oxidation while decreasing insulin resistance that in the end leads to downregulation of SREBP and up-regulation of PPARα and PPARγ , and increased hepatic FA oxidation as well (Soriguer et al., 2006; Assy et al., 2009). However, several other phytochemicals would also contribute to the overall lipotropic effect of olive oil, such as phenolic compounds, squalene, lignans, and hydroxytyrosol, which prompted Assy et al. to suggest that olive oil and, more generally, MUFA-rich foods, are a main contributor to the beneficial effect of the Mediterranean diet in the primary prevention of NAFLD (Assy et al., 2009). In addition to olive oil, PUFA/n-3 rich/low-trans structured fats synthesized from flaxseed oil, butter fat, and palm stearin were also shown to exert significant lipotropic effects. These include a decreased hepatic TG content of 16%, an increased β-oxidation of 96%, and an increased CPT activity of 88% in ApoE−/− mice compared to ApoE−/− mice fed a 10%-fat (commercial shortening, 53.4% trans FAs) diet (Supplemental Table 5; Cho et al., 2009). However, the results do not appear to be consistent."

"Short-chain fatty acids (SCFA) mainly result from fiber fermentation in humans and animals. The most important are acetate, propionate, and butyrate. As for the previously PBF compounds, they have been shown, either as isolated compounds or in a mixture, to exert positive and significant effects on hepatic lipid metabolism (Supplemental Table 2). But only one study reported a significant decrease in hepatic TG content (around 16%) with acetic acid in high-fat fed mice (Kondo et al., 2009). Among themechanisms involved, up-regulation of PPARα, ACO, and CPT-1 and down-regulation of FAS gene expression were demonstrated (Kondo et al., 2009). Consequently, because SCFA are produced via fiber fermentation within the colon, fiber may indirectly play a role in these mechanisms.

Other studies have mainly reported on the inhibition effect of SCFAs upon the rate of cholesterol synthesis, as shown in isolated hepatocytes with propionic acid (Wright et al., 1990) or in liver slices with SCFA mixtures of acetic, propionic, and butyric acids (Hara et al., 1999; Supplemental Table 2). Hepatic acetate and propionate concentrations were also shown to be negatively correlated with hepatic cholesterol content in rats (Koseki et al., 1991)."

"Several studies have reported on the protective effect of melatonin against liver injury in relation to its antioxidant property and on its effect on gene expression in relation to its antioxidant status (Taysi et al., 2003; Leon et al., 2004; Sener et al., 2004; Catala et al., 2007; Subramanian et al., 2007)."

"[..]hazelnuts and walnuts are considered good vegetable sources of melatonin; melatonin is also found in algae, ginger, grapes, cocoa, cereals (e.g., maize, rice, and wheat), tomatoes, potatoes, and green vegetables."

"The physicochemical properties of fiber have to be considered to explain their hepatic lipid-lowering effect. For example, fiber, especially hydrophobic lignin (included in the fiber definition), has been shown to adsorb and/or sequester bile acid conjugates via hydrophobic bonds (Eastwood and Girdwood, 1968; Eastwood and Hamilton, 1968; Eastwood, 1975; Eastwood and Mowbray, 1976), potentially stimulating cholesterol efflux from the liver. Later, Mongeau and Brassard evaluated the bile salt binding capacity of various cereal products and found that they ranged from 16.2 μmol glycocholate/0.2 g of neutral detergent fiber (NDF) for wheat germ to 34.2 μmol glycocholate/0.2 g NDF for spoon-size shredded wheat (Mongeau and Brassard, 1982)."

"Concerning phenolic acids, except for two recent studies that support the presence of a lipotropic effect for ferulic (Son et al., 2010) and protocatechuic acids (Liu et al., 2010), other studies have not shown any significant reduction in hepatic TG content (Supplemental Table 4). However, other markers were improved. For example, gallic acid was shown to have no effect on FAS activity in vitro (Wang et al., 2003). The most significant effect was the inhibition of HMG-CoA reductase by ferulic acid in high-cholesterol fed rats (Kim et al., 2003). In this study, ferulic acid was also shown to significantly reduce acyl- CoA:cholesterol acyltransferase (which forms cholesteryl esters from cholesterol) activity (Kim et al., 2003). However, this is not sufficient to assume that all phenolic acids have lipotropic effects."

"Curcumin is not classified as a polyphenol sensu stricto but may be considered a polyphenol-derived compound (Figure 1). Interestingly, in the two studies reported in Supplemental Table 4, curcumin was shown to significantly decrease the hepatic TG content by 22% in high-cholesterol fed rats (Seetharamaiah and Chandrasekhara, 1993)."

"Caffeine also appears to have lipotropic effects because it is able to significantly reduce hepatic TG content by 29% and to significantly decrease SREBP-1 (∼0.6-fold that of the control) and FAS (∼0.5-fold that of the control) mRNA levels in male KK-Ay mice that spontaneously developed type 2 diabetes (Yamauchi et al., 2010)."

"[..]rather than focus on an isolated compound, more and more studies are being conducted to investigate the effect of ethanol- and/or water-extractable polyphenols from plants on hepatic lipid metabolism in various animal models (Supplemental Table 4)."

"Plant-based foods may contain a whole set of lipotropes. Thus, the effect of foods or of their extracts on steatosis is particularly relevant to study and is closer to the nutritional reality than the study of isolated compounds, which are often used at doses higher than those really consumed by humans."

"Tomato powder significantly reduced (by 22%) the hepatic TG content in rats fed a standard diet, but lycopene alone in the same amount found in the tomato powder had no effect (Alshatwi et al., 2010)."

"We therefore hypothesize that, as with antioxidants, it is preferable to consume complex PBF containing several lipotropes rather than only one lipotrope at a high dose because of their different modes of action toward lipid metabolism in the liver that can compete with each other. The issue of synergism for lipotropes might be well illustrated by the example of niacin, which may be hepatotoxic and produce other harmful side effects (e.g., flushing and nausea) at high doses within a therapeutic context (McKenney et al., 1994), but may be beneficial at lower doses and/or accompanied with other lipotropes such as betaine (McCarty, 2000), choline (Wenru et al., 1994), folates (McCarty, 2000), methionine (Aronov et al., 1999)"

upload_2018-6-30_15-21-4.png
Figures 2A-D are quite interesting but too detailed to include here.
 
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Motif

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Fat-solubles and niacin megadoses, taurine, glycine, lysine, a big amount of coffee and two red bulls a day cleared my liver pretty fast. Before this protocol I could eat the cleanest diet and felt like ***t. Right now I can eat whatever I want and feel just fine, sometimes great. Tobacco was a great help too.


Tobacco? Smoked?
 

SOMO

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They discuss hydroxycitric acid as useful but I'm not familiar with it, so I don't know if it's worth spending time reading about it.

What I know about Hydroxycitric Acid is that it inhibits and limits De Novo Lipogenesis.

Sorry for bumping an old topic, but just in case anyone was curious HCA supposedly limits DNL.
 

GreekDemiGod

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I used to drink several coffees for breakfast with no food, and felt incredible for several hours. It was only years later that I started to feel the negative effects of this, and resolving them has not been easy
What would those long-term effects be?
 

Bart1

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I want to revamp this thread because I also seem to be in this boat. Been doing a Peat inspired diet for over a year. Made a lot of mistakes on the way. One of the things was waiting too long with taking thyroid while taking more and more fructose and sucrose. If you don’t run an oxidative metabolism sugar will increase lactic acid production and also fat will accumulate. So a way out of this is probably lowering stress hormones and get thyroid function up. I’ve been trying high doses of K2 which did work however my nails began to show more serious issues related to renal function. If you pound on liver detox things coffee and K2 , could it be that in the near term kidneys get stressed more ? How to deal with that? We don’t want to create kidney problems as well.
 

Bart1

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On what basis did you decide to take thyroid? Temps, blood tests? What was your TSH?
Temps, Pulse and symptoms of hypothyroidism. My TSH wasn't actually that high, around 1.6. I did do some extra tests like reverse T3 which showed an elevation. This was for me an extra confirmation I had liver and gut issues and wasn't converting thyroid properly
 
OP
Tarmander

Tarmander

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Apr 30, 2015
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I want to revamp this thread because I also seem to be in this boat. Been doing a Peat inspired diet for over a year. Made a lot of mistakes on the way. One of the things was waiting too long with taking thyroid while taking more and more fructose and sucrose. If you don’t run an oxidative metabolism sugar will increase lactic acid production and also fat will accumulate. So a way out of this is probably lowering stress hormones and get thyroid function up. I’ve been trying high doses of K2 which did work however my nails began to show more serious issues related to renal function. If you pound on liver detox things coffee and K2 , could it be that in the near term kidneys get stressed more ? How to deal with that? We don’t want to create kidney problems as well.
yeah detoxing the liver stresses the kidneys. What stabilizes the kidneys is stability in your life. Think of it like a water hose. The faster you live, the more chaotic, the more that hose goes from nothing to firehose, and back and forth. This messes the kidneys up.
 

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